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Extracellular Interactors of the IGF System: Impact on Cancer Hallmarks and Therapeutic Approaches
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The Relationship between Circadian Rhythm and Cancer Disease
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Exploring the Immunological Profile in Breast Cancer: Recent Advances in Diagnosis and Prognosis through Circulating Tumor Cells
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Molecularly Imprinted Drug Carrier for Lamotrigine—Design, Synthesis, and Characterization of Physicochemical Parameters
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Radiocarbon Flux Measurements Provide Insight into Why a Pyroligneous Acid Product Stimulates Plant Growth
Journal Description
International Journal of Molecular Sciences
International Journal of Molecular Sciences
is an international, peer-reviewed, open access journal providing an advanced forum for biochemistry, molecular and cell biology, molecular biophysics, molecular medicine, and all aspects of molecular research in chemistry, and is published semimonthly online by MDPI. The Australian Society of Plant Scientists (ASPS), Epigenetics Society, European Calcium Society (ECS), European Chitin Society (EUCHIS), Spanish Society for Cell Biology (SEBC) and others are affiliated with IJMS and their members receive a discount on the article processing charges.
- Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
- High Visibility: indexed within Scopus, SCIE (Web of Science), PubMed, PMC, MEDLINE, Embase, CAPlus / SciFinder, and other databases.
- Journal Rank: JCR - Q1 (Biochemistry and Molecular Biology) / CiteScore - Q1 (Inorganic Chemistry)
- Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 18.1 days after submission; acceptance to publication is undertaken in 2.8 days (median values for papers published in this journal in the first half of 2024).
- Recognition of Reviewers: reviewers who provide timely, thorough peer-review reports receive vouchers entitling them to a discount on the APC of their next publication in any MDPI journal, in appreciation of the work done.
- Testimonials: See what our editors and authors say about the IJMS.
- Companion journals for IJMS include: Biophysica, Obesities, Stresses and Lymphatics.
Impact Factor:
4.9 (2023);
5-Year Impact Factor:
5.6 (2023)
Latest Articles
Lipids and Lipid-Mediated Signaling in Plant–Pathogen Interactions
Int. J. Mol. Sci. 2024, 25(13), 7255; https://doi.org/10.3390/ijms25137255 (registering DOI) - 1 Jul 2024
Abstract
Plant lipids are essential cell constituents with many structural, storage, signaling, and defensive functions. During plant–pathogen interactions, lipids play parts in both the preexisting passive defense mechanisms and the pathogen-induced immune responses at the local and systemic levels. They interact with various components
[...] Read more.
Plant lipids are essential cell constituents with many structural, storage, signaling, and defensive functions. During plant–pathogen interactions, lipids play parts in both the preexisting passive defense mechanisms and the pathogen-induced immune responses at the local and systemic levels. They interact with various components of the plant immune network and can modulate plant defense both positively and negatively. Under biotic stress, lipid signaling is mostly associated with oxygenated natural products derived from unsaturated fatty acids, known as oxylipins; among these, jasmonic acid has been of great interest as a specific mediator of plant defense against necrotrophic pathogens. Although numerous studies have documented the contribution of oxylipins and other lipid-derived species in plant immunity, their specific roles in plant–pathogen interactions and their involvement in the signaling network require further elucidation. This review presents the most relevant and recent studies on lipids and lipid-derived signaling molecules involved in plant–pathogen interactions, with the aim of providing a deeper insight into the mechanisms underpinning lipid-mediated regulation of the plant immune system.
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(This article belongs to the Section Molecular Plant Sciences)
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PIEZO1 Promotes the Migration of Endothelial Cells via Enhancing CXCR4 Expression under Simulated Microgravity
by
Yuan Wang, Chengfei Li, Ruonan Wang, **ngcheng Zhao, Yikai Pan, Qian Zhang, Shuhan Li, Jieyi Fan, Yongchun Wang and **qing Sun
Int. J. Mol. Sci. 2024, 25(13), 7254; https://doi.org/10.3390/ijms25137254 (registering DOI) - 1 Jul 2024
Abstract
Exposure to microgravity during spaceflight induces the alterations in endothelial cell function associated with post-flight cardiovascular deconditioning. PIEZO1 is a major mechanosensitive ion channel that regulates endothelial cell function. In this study, we used a two-dimensional clinostat to investigate the expression of PIEZO1
[...] Read more.
Exposure to microgravity during spaceflight induces the alterations in endothelial cell function associated with post-flight cardiovascular deconditioning. PIEZO1 is a major mechanosensitive ion channel that regulates endothelial cell function. In this study, we used a two-dimensional clinostat to investigate the expression of PIEZO1 and its regulatory mechanism on human umbilical vein endothelial cells (HUVECs) under simulated microgravity. Utilizing quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis, we observed that PIEZO1 expression was significantly increased in response to simulated microgravity. Moreover, we found microgravity promoted endothelial cells migration by increasing expression of PIEZO1. Proteomics analysis highlighted the importance of C-X-C chemokine receptor type 4(CXCR4) as a main target molecule of PIEZO1 in HUVECs. CXCR4 protein level was increased with simulated microgravity and decreased with PIEZO1 knock down. The mechanistic study showed that PIEZO1 enhances CXCR4 expression via Ca2+ influx. In addition, CXCR4 could promote endothelial cell migration under simulated microgravity. Taken together, these results suggest that the upregulation of PIEZO1 in response to simulated microgravity regulates endothelial cell migration due to enhancing CXCR4 expression via Ca2+ influx.
Full article
(This article belongs to the Section Molecular Biology)
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Open AccessArticle
Deletion of the Mitochondrial Membrane Protein Fam210b Is Associated with the Development of Systemic Lupus Erythematosus
by
Yaqi Xu, Ran Gao, Min Zhang, Qi Zeng, Gaizhi Zhu, **ming Qiu, Wenting Su and Renxi Wang
Int. J. Mol. Sci. 2024, 25(13), 7253; https://doi.org/10.3390/ijms25137253 (registering DOI) - 1 Jul 2024
Abstract
Mitochondrial dysfunction has been increasingly recognized as a trigger for systemic lupus erythematosus (SLE). Recent bioinformatics studies have suggested Fam210b as a significant candidate for the classification and therapeutic targeting of SLE. To experimentally prove the role of Fam210b in SLE, we constructed
[...] Read more.
Mitochondrial dysfunction has been increasingly recognized as a trigger for systemic lupus erythematosus (SLE). Recent bioinformatics studies have suggested Fam210b as a significant candidate for the classification and therapeutic targeting of SLE. To experimentally prove the role of Fam210b in SLE, we constructed Fam210b knockout (Fam210b−/−) mice using the CRISPR-Cas9 method. We found that approximately 15.68% of Fam210b−/− mice spontaneously developed lupus-like autoimmunity, which was characterized by skin ulcerations, splenomegaly, and an increase in anti-double-stranded DNA (anti-dsDNA) IgG antibodies and anti-nuclear antibodies(ANA). Single-cell sequencing showed that Fam210b was mainly expressed in erythroid cells. Critically, the knockout of Fam210b resulted in abnormal erythrocyte differentiation and development in the spleens of mice. Concurrently, the spleens exhibited an increased number of CD71+ erythroid cells, along with elevated levels of reactive oxygen species (ROS) in the erythrocytes. The co-culture of CD71+ erythroid cells and lymphocytes resulted in lymphocyte activation and promoted dsDNA and IgG production. In summary, Fam210b knockout leads to a low probability of lupus-like symptoms in mice through the overproduction of ROS in CD71+ erythroid cells. Thus, Fam210b reduction may serve as a novel key marker that triggers the development of SLE.
Full article
(This article belongs to the Special Issue New Insights in Biomarkers of Autoimmune and Autoinflammatory Diseases)
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Open AccessReview
Genomic and Epigenomic Biomarkers of Immune Checkpoint Immunotherapy Response in Melanoma: Current and Future Perspectives
by
Sultana Mehbuba Hossain, Carien Carpenter and Michael R. Eccles
Int. J. Mol. Sci. 2024, 25(13), 7252; https://doi.org/10.3390/ijms25137252 (registering DOI) - 30 Jun 2024
Abstract
Immune checkpoint inhibitors (ICIs) demonstrate durable responses, long-term survival benefits, and improved outcomes in cancer patients compared to chemotherapy. However, the majority of cancer patients do not respond to ICIs, and a high proportion of those patients who do respond to ICI therapy
[...] Read more.
Immune checkpoint inhibitors (ICIs) demonstrate durable responses, long-term survival benefits, and improved outcomes in cancer patients compared to chemotherapy. However, the majority of cancer patients do not respond to ICIs, and a high proportion of those patients who do respond to ICI therapy develop innate or acquired resistance to ICIs, limiting their clinical utility. The most studied predictive tissue biomarkers for ICI response are PD-L1 immunohistochemical expression, DNA mismatch repair deficiency, and tumour mutation burden, although these are weak predictors of ICI response. The identification of better predictive biomarkers remains an important goal to improve the identification of patients who would benefit from ICIs. Here, we review established and emerging biomarkers of ICI response, focusing on epigenomic and genomic alterations in cancer patients, which have the potential to help guide single-agent ICI immunotherapy or ICI immunotherapy in combination with other ICI immunotherapies or agents. We briefly review the current status of ICI response biomarkers, including investigational biomarkers, and we present insights into several emerging and promising epigenomic biomarker candidates, including current knowledge gaps in the context of ICI immunotherapy response in melanoma patients.
Full article
(This article belongs to the Special Issue Melanoma: From Molecular Pathology to Therapeutic Approaches)
Open AccessArticle
Selective Assembly of TRPC Channels in the Rat Retina during Photoreceptor Degeneration
by
Elena Caminos, Susana López-López and Juan R. Martinez-Galan
Int. J. Mol. Sci. 2024, 25(13), 7251; https://doi.org/10.3390/ijms25137251 (registering DOI) - 30 Jun 2024
Abstract
Transient receptor potential canonical (TRPC) channels are calcium channels with diverse expression profiles and physiological implications in the retina. Neurons and glial cells of rat retinas with photoreceptor degeneration caused by retinitis pigmentosa (RP) exhibit basal calcium levels that are above those detected
[...] Read more.
Transient receptor potential canonical (TRPC) channels are calcium channels with diverse expression profiles and physiological implications in the retina. Neurons and glial cells of rat retinas with photoreceptor degeneration caused by retinitis pigmentosa (RP) exhibit basal calcium levels that are above those detected in healthy retinas. Inner retinal cells are the last to degenerate and are responsible for maintaining the activity of the visual cortex, even after complete loss of photoreceptors. We considered the possibility that TRPC1 and TRPC5 channels might be associated with both the high calcium levels and the delay in inner retinal degeneration. TRPC1 is known to mediate protective effects in neurodegenerative processes while TRPC5 promotes cell death. In order to comprehend the implications of these channels in RP, the co-localization and subsequent physical interaction between TRPC1 and TRPC5 in healthy retina (Sprague-Dawley rats) and degenerating (P23H-1, a model of RP) retina were detected by immunofluorescence and proximity ligation assays. There was an overlap** signal in the innermost retina of all animals where TRPC1 and TRPC5 physically interacted. This interaction increased significantly as photoreceptor loss progressed. Both channels function as TRPC1/5 heteromers in the healthy and damaged retina, with a marked function of TRPC1 in response to retinal degenerative mechanisms. Furthermore, our findings support that TRPC5 channels also function in partnership with STIM1 in Müller and retinal ganglion cells. These results suggest that an increase in TRPC1/5 heteromers may contribute to the slowing of the degeneration of the inner retina during the outer retinal degeneration.
Full article
(This article belongs to the Special Issue TRP Channels in Physiology and Pathophysiology 2.0)
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Open AccessArticle
Region-Specific Effects of Metformin on Gut Microbiome and Metabolome in High-Fat Diet-Induced Type 2 Diabetes Mouse Model
by
Meihui Cheng, **anxian Jia, Lili Ren, Siqian Chen, Wei Wang, Jianwei Wang and Bin Cong
Int. J. Mol. Sci. 2024, 25(13), 7250; https://doi.org/10.3390/ijms25137250 (registering DOI) - 30 Jun 2024
Abstract
The glucose-lowering drug metformin alters the composition of the gut microbiome in patients with type 2 diabetes mellitus (T2DM) and other diseases. Nevertheless, most studies on the effects of this drug have relied on fecal samples, which provide limited insights into its local
[...] Read more.
The glucose-lowering drug metformin alters the composition of the gut microbiome in patients with type 2 diabetes mellitus (T2DM) and other diseases. Nevertheless, most studies on the effects of this drug have relied on fecal samples, which provide limited insights into its local effects on different regions of the gut. Using a high-fat diet (HFD)-induced mouse model of T2DM, we characterize the spatial variability of the gut microbiome and associated metabolome in response to metformin treatment. Four parts of the gut as well as the feces were analyzed using full-length sequencing of 16S rRNA genes and targeted metabolomic analyses, thus providing insights into the composition of the microbiome and associated metabolome. We found significant differences in the gut microbiome and metabolome in each gut region, with the most pronounced effects on the microbiomes of the cecum, colon, and feces, with a significant increase in a variety of species belonging to Akkermansiaceae, Lactobacillaceae, Tannerellaceae, and Erysipelotrichaceae. Metabolomics analysis showed that metformin had the most pronounced effect on microbiome-derived metabolites in the cecum and colon, with several metabolites, such as carbohydrates, fatty acids, and benzenoids, having elevated levels in the colon; however, most of the metabolites were reduced in the cecum. Thus, a wide range of beneficial metabolites derived from the microbiome after metformin treatment were produced mainly in the colon. Our study highlights the importance of considering gut regions when understanding the effects of metformin on the gut microbiome and metabolome.
Full article
(This article belongs to the Section Molecular Pharmacology)
Open AccessArticle
Integrative Analysis of Hepatopancreas Transcriptome and Proteome in Female Eriocheir sinensis under Thermal Stress
by
Tingshuang Pan, Tong Li, Min Yang, He Jiang and Jun Ling
Int. J. Mol. Sci. 2024, 25(13), 7249; https://doi.org/10.3390/ijms25137249 (registering DOI) - 30 Jun 2024
Abstract
The Chinese mitten crab (Eriocheir sinensis), an economically important crustacean that is endemic to China, has recently experienced high-temperature stress. The high thermal tolerance of E. sinensis points to its promise in being highly productive in an aquacultural context. However, the
[...] Read more.
The Chinese mitten crab (Eriocheir sinensis), an economically important crustacean that is endemic to China, has recently experienced high-temperature stress. The high thermal tolerance of E. sinensis points to its promise in being highly productive in an aquacultural context. However, the mechanisms underlying its high thermal tolerance remain unknown. In this study, female E. sinensis that were heat exposed for 24 h at 38.5°C and 33°C were identified as high-temperature-stressed (HS) and normal-temperature-stressed (NS) groups, respectively. The hepatopancreas of E. sinensis from the HS and NS groups were used for transcriptome and proteomic analyses. A total of 2350 upregulated and 1081 downregulated differentially expressed genes (DEGs) were identified between the HS and NS groups. In addition, 126 differentially expressed proteins (DEPs) were upregulated and 35 were downregulated in the two groups. An integrated analysis showed that 2641 identified genes were correlated with their corresponding proteins, including 25 genes that were significantly differentially expressed between the two omics levels. Ten Gene Ontology terms were enriched in the DEGs and DEPs. A functional analysis revealed three common pathways that were significantly enriched in both DEGs and DEPs: fluid shear stress and atherosclerosis, leukocyte transendothelial migration, and thyroid hormone synthesis. Further analysis of the common pathways showed that MGST1, Act5C, HSP90AB1, and mys were overlap** genes at the transcriptome and proteome levels. These results demonstrate the differences between the HS and NS groups at the two omics levels and will be helpful in clarifying the mechanisms underlying the thermal tolerance of E. sinensis.
Full article
(This article belongs to the Section Molecular Biology)
Open AccessArticle
Broadening the Genetic Spectrum of Painful Small-Fiber Neuropathy through Whole-Exome Study in Early-Onset Cases
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Kaalindi Misra, Milena Ślęczkowska, Silvia Santoro, Monique M. Gerrits, Elisabetta Mascia, Margherita Marchi, Erika Salvi, Hubert J. M. Smeets, Janneke G. J. Hoeijmakers, Filippo Giovanni Martinelli Boneschi, Massimo Filippi, Giuseppe Lauria Pinter, Catharina G. Faber and Federica Esposito
Int. J. Mol. Sci. 2024, 25(13), 7248; https://doi.org/10.3390/ijms25137248 (registering DOI) - 30 Jun 2024
Abstract
Small-Fiber Neuropathy (SFN) is a disorder of the peripheral nervous system, characterised by neuropathic pain; approximately 11% of cases are linked to variants in Voltage-Gated Sodium Channels (VGSCs). This study aims to broaden the genetic knowledge on painful SFN by applying Whole-Exome Sequencing
[...] Read more.
Small-Fiber Neuropathy (SFN) is a disorder of the peripheral nervous system, characterised by neuropathic pain; approximately 11% of cases are linked to variants in Voltage-Gated Sodium Channels (VGSCs). This study aims to broaden the genetic knowledge on painful SFN by applying Whole-Exome Sequencing (WES) in Early-Onset (EO) cases. A total of 88 patients from Italy (n = 52) and the Netherlands (n = 36), with a disease onset at age ≤ 45 years old and a Pain Numerical Rating Score ≥ 4, were recruited. After variant filtering and classification, WES analysis identified 142 potentially causative variants in 93 genes; 8 are Pathogenic, 15 are Likely Pathogenic, and 119 are Variants of Uncertain Significance. Notably, an enrichment of variants in transient receptor potential genes was observed, suggesting their role in pain modulation alongside VGSCs. A pathway analysis performed by comparing EO cases with 40 Italian healthy controls found enriched mutated genes in the “Nicotinic acetylcholine receptor signaling pathway”. Targeting this pathway with non-opioid drugs could offer novel therapeutic avenues for painful SFN. Additionally, with this study we demonstrated that employing a gene panel of reported mutated genes could serve as an initial screening tool for SFN in genetic studies, enhancing clinical diagnostics.
Full article
(This article belongs to the Special Issue New Insights into the Molecular Mechanisms of Chronic Pain)
Open AccessArticle
Korean Black Goat Extract Exerts Estrogen-like Osteoprotective Effects by Stimulating Osteoblast Differentiation in MC3T3-E1 Cells and Suppressing Osteoclastogenesis in RAW 264.7 Cells
by
Reshmi Akter, ** Sung Son, Jong Chan Ahn, Md Niaj Morshed, Gyong Jai Lee, Min Jun Kim, Jeong Taek An, Byoung Man Kong, Joong-Hyun Song, Deok Chun Yang, Muhammad Awais and Dong Uk Yang
Int. J. Mol. Sci. 2024, 25(13), 7247; https://doi.org/10.3390/ijms25137247 (registering DOI) - 30 Jun 2024
Abstract
Postmenopausal osteoporosis, characterized by an imbalance between osteoclast-mediated bone resorption and osteoblast-driven bone formation, presents substantial health implications. In this study, we investigated the role of black goat extract (BGE), derived from a domesticated native Korean goat, estrogen-like activity, and osteoprotective effects in
[...] Read more.
Postmenopausal osteoporosis, characterized by an imbalance between osteoclast-mediated bone resorption and osteoblast-driven bone formation, presents substantial health implications. In this study, we investigated the role of black goat extract (BGE), derived from a domesticated native Korean goat, estrogen-like activity, and osteoprotective effects in vitro. BGE’s mineral and fatty acid compositions were analyzed via the ICP-AES method and gas chromatography–mass spectrometry, respectively. In vitro experiments were conducted using MCF-7 breast cancer cells, MC3T3-E1 osteoblasts, and RAW264.7 osteoclasts. BGE exhibits a favorable amount of mineral and fatty acid content. It displayed antimenopausal activity by stimulating MCF-7 cell proliferation and augmenting estrogen-related gene expression (ERα, ERβ, and pS2). Moreover, BGE positively impacted osteogenesis and mineralization in MC3T3-E1 cells through Wnt/β-catenin pathway modulation, leading to heightened expression of Runt-related transcription factor 2, osteoprotegerin, and collagen type 1. Significantly, BGE effectively suppressed osteoclastogenesis by curtailing osteoclast formation and activity in RAW264.7 cells, concurrently downregulating pivotal signaling molecules, including receptor activator of nuclear factor κ B and tumor necrosis factor receptor-associated factor 6. This study offers a shred of preliminary evidence for the prospective use of BGE as an effective postmenopausal osteoporosis treatment.
Full article
(This article belongs to the Section Molecular Pharmacology)
Open AccessArticle
Differential Regulation of Hemichannels and Gap Junction Channels by RhoA GTPase and Actin Cytoskeleton: A Comparative Analysis of Cx43 and Cx26
by
Oscar Jara, Jaime Maripillán, Fanny Momboisse, Ana María Cárdenas, Isaac E. García and Agustín D. Martínez
Int. J. Mol. Sci. 2024, 25(13), 7246; https://doi.org/10.3390/ijms25137246 (registering DOI) - 30 Jun 2024
Abstract
Connexins (Cxs) are transmembrane proteins that assemble into gap junction channels (GJCs) and hemichannels (HCs). Previous researches support the involvement of Rho GTPases and actin microfilaments in the trafficking of Cxs, formation of GJCs plaques, and regulation of channel activity. Nonetheless, it remains
[...] Read more.
Connexins (Cxs) are transmembrane proteins that assemble into gap junction channels (GJCs) and hemichannels (HCs). Previous researches support the involvement of Rho GTPases and actin microfilaments in the trafficking of Cxs, formation of GJCs plaques, and regulation of channel activity. Nonetheless, it remains uncertain whether distinct types of Cxs HCs and GJCs respond differently to Rho GTPases or changes in actin polymerization/depolymerization dynamics. Our investigation revealed that inhibiting RhoA, a small GTPase that controls actin polymerization, or disrupting actin microfilaments with cytochalasin B (Cyto-B), resulted in reduced GJCs plaque size at appositional membranes and increased transport of HCs to non-appositional plasma membrane regions. Notably, these effects were consistent across different Cx types, since Cx26 and Cx43 exhibited similar responses, despite having distinct trafficking routes to the plasma membrane. Functional assessments showed that RhoA inhibition and actin depolymerization decreased the activity of Cx43 GJCs while significantly increasing HC activity. However, the functional status of GJCs and HCs composed of Cx26 remained unaffected. These results support the hypothesis that RhoA, through its control of the actin cytoskeleton, facilitates the transport of HCs to appositional cell membranes for GJCs formation while simultaneously limiting the positioning of free HCs at non-appositional cell membranes, independently of Cx type. This dynamic regulation promotes intercellular communications and reduces non-selective plasma membrane permeability through a Cx-type dependent mechanism, whereby the activity of Cx43 HCs and GJCs are differentially affected but Cx26 channels remain unchanged.
Full article
(This article belongs to the Section Biochemistry)
Open AccessArticle
The Characterization of a Novel PrMADS11 Transcription Factor from Pinus radiata Induced Early in Bent Pine Stem
by
Tamara Méndez, Joselin Guajardo, Nicolás Cruz, Rodrigo A. Gutiérrez, Lorena Norambuena, Andrea Vega, María A. Moya-León and Raúl Herrera
Int. J. Mol. Sci. 2024, 25(13), 7245; https://doi.org/10.3390/ijms25137245 (registering DOI) - 30 Jun 2024
Abstract
A novel MADS-box transcription factor from Pinus radiata D. Don was characterized. PrMADS11 encodes a protein of 165 amino acids for a MADS-box transcription factor belonging to group II, related to the MIKC protein structure. PrMADS11 was differentially expressed in the stems of
[...] Read more.
A novel MADS-box transcription factor from Pinus radiata D. Don was characterized. PrMADS11 encodes a protein of 165 amino acids for a MADS-box transcription factor belonging to group II, related to the MIKC protein structure. PrMADS11 was differentially expressed in the stems of pine trees in response to 45° inclination at early times (1 h). Arabidopsis thaliana was stably transformed with a 35S::PrMADS11 construct in an effort to identify the putative targets of PrMADS11. A massive transcriptome analysis revealed 947 differentially expressed genes: 498 genes were up-regulated, and 449 genes were down-regulated due to the over-expression of PrMADS11. The gene ontology analysis highlighted a cell wall remodeling function among the differentially expressed genes, suggesting the active participation of cell wall modification required during the response to vertical stem loss. In addition, the phenylpropanoid pathway was also indicated as a PrMADS11 target, displaying a marked increment in the expression of the genes driven to the biosynthesis of monolignols. The EMSA assays confirmed that PrMADS11 interacts with CArG-box sequences. This TF modulates the gene expression of several molecular pathways, including other TFs, as well as the genes involved in cell wall remodeling. The increment in the lignin content and the genes involved in cell wall dynamics could be an indication of the key role of PrMADS11 in the response to trunk inclination.
Full article
(This article belongs to the Special Issue Transcription Factors in Plant Gene Expression Regulation)
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Open AccessArticle
Comparative Phenotypic and Transcriptomic Analyses Provide Novel Insights into the Molecular Mechanism of Seed Germination in Response to Low Temperature Stress in Alfalfa
by
Zhao Zhang, Yanzhen Lv, Qingying Sun, **ngjie Yao and Huifang Yan
Int. J. Mol. Sci. 2024, 25(13), 7244; https://doi.org/10.3390/ijms25137244 (registering DOI) - 30 Jun 2024
Abstract
Low temperature is the most common abiotic factor that usually occurs during the seed germination of alfalfa (Medicago sativa L.). However, the potential regulatory mechanisms involved in alfalfa seed germination under low temperature stress are still ambiguous. Therefore, to determine the relevant
[...] Read more.
Low temperature is the most common abiotic factor that usually occurs during the seed germination of alfalfa (Medicago sativa L.). However, the potential regulatory mechanisms involved in alfalfa seed germination under low temperature stress are still ambiguous. Therefore, to determine the relevant key genes and pathways, the phenotypic and transcriptomic analyses of low-temperature sensitive (Instict) and low-temperature tolerant (Sardi10) alfalfa were conducted at 6 and 15 h of seed germination under normal (20 °C) and low (10 °C) temperature conditions. Germination phenotypic results showed that Sardi10 had the strongest germination ability under low temperatures, which was manifested by the higher germination-related indicators. Further transcriptome analysis indicated that differentially expressed genes were mainly enriched in galactose metabolism and carbon metabolism pathways, which were the most commonly enriched in two alfalfa genotypes. Additionally, fatty acid metabolism and glutathione metabolism pathways were preferably enriched in Sardi10 alfalfa. The Weighted Gene Co-Expression Network Analysis (WGCNA) suggested that genes were closely related to galactose metabolism, fatty acid metabolism, and glutathione metabolism in Sardi10 alfalfa at the module with the highest correlation (6 h of germination under low temperature). Finally, qRT-PCR analysis further validated the related genes involved in the above pathways, which might play crucial roles in regulating seed germination of alfalfa under low temperature conditions. These findings provide new insights into the molecular mechanisms of seed germination underlying the low temperature stress in alfalfa.
Full article
(This article belongs to the Section Molecular Plant Sciences)
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Open AccessArticle
Lipid Emulsions Inhibit Labetalol-Induced Vasodilation in the Isolated Rat Aorta
by
Soohee Lee, Kyeong-Eon Park, Yeran Hwang, Sungil Bae, Seong-Ho Ok, Seung-Hyun Ahn, Gyu** Sim, Hyun-** Kim, Seunghyeon Park and Ju-Tae Sohn
Int. J. Mol. Sci. 2024, 25(13), 7243; https://doi.org/10.3390/ijms25137243 (registering DOI) - 30 Jun 2024
Abstract
Lipid emulsions are used as adjuvant drugs to alleviate intractable cardiovascular collapse induced by drug toxicity. We aimed to examine the effect of lipid emulsions on labetalol-induced vasodilation and the underlying mechanism in the isolated rat aorta. We studied the effects of endothelial
[...] Read more.
Lipid emulsions are used as adjuvant drugs to alleviate intractable cardiovascular collapse induced by drug toxicity. We aimed to examine the effect of lipid emulsions on labetalol-induced vasodilation and the underlying mechanism in the isolated rat aorta. We studied the effects of endothelial denudation, NW-nitro-l-arginine methyl ester (l-NAME), calmidazolium, methylene blue, 1H-[1,2,4]oxadiazolo[4,3-a] quinoxalin-1-one (ODQ), and lipid emulsions on labetalol-induced vasodilation. We also evaluated the effects of lipid emulsions on cyclic guanosine monophosphate (cGMP) formation, endothelial nitric oxide synthase (eNOS) phosphorylation, and endothelial calcium levels induced by labetalol. Labetalol-induced vasodilation was higher in endothelium-intact aortas than that in endothelium-denuded aortas. l-NAME, calmidazolium, methylene blue, and ODQ inhibited labetalol-induced vasodilation in endothelium-intact aortas. Lipid emulsions inhibited labetalol-induced vasodilation in endothelium-intact and endothelium-denuded aortas. l-NAME, ODQ, and lipid emulsions inhibited labetalol-induced cGMP formation in endothelium-intact aortas. Lipid emulsions reversed the stimulatory and inhibitory eNOS (Ser1177 and Thr495) phosphorylation induced by labetalol in human umbilical vein endothelial cells and inhibited the labetalol-induced endothelial calcium increase. Moreover, it decreased labetalol concentration. These results suggest that lipid emulsions inhibit vasodilation induced by toxic doses of labetalol, which is mediated by the inhibition of endothelial nitric oxide release and reduction of labetalol concentration.
Full article
(This article belongs to the Special Issue Molecular and Translational Research in Cardiovascular Endocrinology, Cardio-Metabolic Diseases and Non-alcoholic Fatty Liver Disease (NAFLD): 2nd Edition)
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Open AccessArticle
UniCAR T-Cell Potency—A Matter of Affinity between Adaptor Molecules and Adaptor CAR T-Cells?
by
Hugo Boutier, Liliana R. Loureiro, Lydia Hoffmann, Claudia Arndt, Tabea Bartsch, Anja Feldmann and Michael P. Bachmann
Int. J. Mol. Sci. 2024, 25(13), 7242; https://doi.org/10.3390/ijms25137242 (registering DOI) - 30 Jun 2024
Abstract
Although Chimeric Antigen Receptor (CAR) T-cells have shown high efficacy in hematologic malignancies, they can cause severe to life-threatening side effects. To address these safety concerns, we have developed adaptor CAR platforms, like the UniCAR system. The redirection of UniCAR T-cells to target
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Although Chimeric Antigen Receptor (CAR) T-cells have shown high efficacy in hematologic malignancies, they can cause severe to life-threatening side effects. To address these safety concerns, we have developed adaptor CAR platforms, like the UniCAR system. The redirection of UniCAR T-cells to target cells relies on a Target Module (TM), containing the E5B9 epitope and a tumor-specific binding moiety. Appropriate UniCAR-T activation thus involves two interactions: between the TM and the CAR T-cell, and the TM and the target cell. Here, we investigate if and how alterations of the amino acid sequence of the E5B9 UniCAR epitope impact the interaction between TMs and the UniCAR. We identify the new epitope E5B9L, for which the monoclonal antibody 5B9 has the greatest affinity. We then integrate the E5B9L peptide in previously established TMs directed to Fibroblast Activation Protein (FAP) and assess if such changes in the UniCAR epitope of the TMs affect UniCAR T-cell potency. Binding properties of the newly generated anti-FAP-E5B9L TMs to UniCAR and their ability to redirect UniCAR T-cells were compared side-by-side with the ones of anti-FAP-E5B9 TMs. Despite a substantial variation in the affinity of the different TMs to the UniCAR, no significant differences were observed in the cytotoxic and cytokine-release profiles of the redirected T-cells. Overall, our work indicates that increasing affinity of the UniCAR to the TM does not play a crucial role in such adaptor CAR system, as it does not significantly impact the potency of the UniCAR T-cells.
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(This article belongs to the Special Issue Adapter CAR T Cells: From the Idea to the Clinic)
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Open AccessArticle
Assessment of the Biocompatibility Ability and Differentiation Capacity of Mesenchymal Stem Cells on Biopolymer/Gold Nanocomposites
by
Huey-Shan Hung, Chiung-Chyi Shen, Jyun-Ting Wu, Chun-Yu Yueh, Meng-Yin Yang, Yi-Chin Yang and Wen-Yu Cheng
Int. J. Mol. Sci. 2024, 25(13), 7241; https://doi.org/10.3390/ijms25137241 (registering DOI) - 30 Jun 2024
Abstract
This study assessed the biocompatibility of two types of nanogold composites: fibronectin-gold (FN-Au) and collagen-gold (Col-Au). It consisted of three main parts: surface characterization, in vitro biocompatibility assessments, and animal models. To determine the structural and functional differences between the materials used in
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This study assessed the biocompatibility of two types of nanogold composites: fibronectin-gold (FN-Au) and collagen-gold (Col-Au). It consisted of three main parts: surface characterization, in vitro biocompatibility assessments, and animal models. To determine the structural and functional differences between the materials used in this study, atomic force microscopy, Fourier-transform infrared spectroscopy, and ultraviolet-visible spectrophotometry were used to investigate their surface topography and functional groups. The F-actin staining, proliferation, migration, reactive oxygen species generation, platelet activation, and monocyte activation of mesenchymal stem cells (MSCs) cultured on the FN-Au and Col-Au nanocomposites were investigated to determine their biological and cellular behaviors. Additionally, animal biocompatibility experiments measured capsule formation and collagen deposition in female Sprague–Dawley rats. The results showed that MSCs responded better on the FN-Au and Col-AU nanocomposites than on the control (tissue culture polystyrene) or pure substances, attributed to their incorporation of an optimal Au concentration (12.2 ppm), which induced significant surface morphological changes, nano topography cues, and better biocompatibility. Moreover, neuronal, endothelial, bone, and adipose tissues demonstrated better differentiation ability on the FN-Au and Col-Au nanocomposites. Nanocomposites have a crucial role in tissue engineering and even vascular grafts. Finally, MSCs were demonstrated to effectively enhance the stability of the endothelial structure, indicating that they can be applied as promising alternatives to clinics in the future.
Full article
(This article belongs to the Section Molecular Nanoscience)
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Open AccessArticle
Creation of an Isogenic Human iPSC-Based RGC Model of Dominant Optic Atrophy Harboring the Pathogenic Variant c.1861C>T (p.Gln621Ter) in the OPA1 Gene
by
Marta García-López, Lydia Jiménez-Vicente, Raquel González-Jabardo, Helena Dorado, Irene Gómez-Manjón, Miguel Ángel Martín, Carmen Ayuso, Joaquín Arenas and María Esther Gallardo
Int. J. Mol. Sci. 2024, 25(13), 7240; https://doi.org/10.3390/ijms25137240 (registering DOI) - 30 Jun 2024
Abstract
Autosomal dominant optic atrophy (ADOA) is a rare progressive disease mainly caused by mutations in OPA1, a nuclear gene encoding for a mitochondrial protein that plays an essential role in mitochondrial dynamics, cell survival, oxidative phosphorylation, and mtDNA maintenance. ADOA is characterized
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Autosomal dominant optic atrophy (ADOA) is a rare progressive disease mainly caused by mutations in OPA1, a nuclear gene encoding for a mitochondrial protein that plays an essential role in mitochondrial dynamics, cell survival, oxidative phosphorylation, and mtDNA maintenance. ADOA is characterized by the degeneration of retinal ganglion cells (RGCs). This causes visual loss, which can lead to legal blindness in many cases. Nowadays, there is no effective treatment for ADOA. In this article, we have established an isogenic human RGC model for ADOA using iPSC technology and the genome editing tool CRISPR/Cas9 from a previously generated iPSC line of an ADOA plus patient harboring the pathogenic variant NM_015560.3: c.1861C>T (p.Gln621Ter) in heterozygosis in OPA1. To this end, a protocol based on supplementing the iPSC culture media with several small molecules and defined factors trying to mimic embryonic development has been employed. Subsequently, the created model was validated, confirming the presence of a defect of intergenomic communication, impaired mitochondrial respiration, and an increase in apoptosis and ROS generation. Finally, we propose the analysis of OPA1 expression by qPCR as an easy read-out method to carry out future drug screening studies using the created RGC model. In summary, this model provides a useful platform for further investigation of the underlying pathophysiological mechanisms of ADOA plus and for testing compounds with potential pharmacological action.
Full article
(This article belongs to the Special Issue Frontiers on Induced Pluripotent Stem Cells (iPSCs))
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Open AccessArticle
Dietary Walnuts Prevented Indomethacin-Induced Gastric Damage via AP-1 Transcribed 15-PGDH, Nrf2-Mediated HO-1, and n-3 PUFA-Derived Resolvin E1
by
Jong Min Park and Ki Baik Hahm
Int. J. Mol. Sci. 2024, 25(13), 7239; https://doi.org/10.3390/ijms25137239 (registering DOI) - 30 Jun 2024
Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs), the most highly prescribed drugs in the world for the treatment of pain, inflammation, and fever, cause gastric mucosal damage, including ulcers, directly or indirectly, by which the development of GI-safer (-sparing) NSAIDs relates to unmet medical needs. This
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Non-steroidal anti-inflammatory drugs (NSAIDs), the most highly prescribed drugs in the world for the treatment of pain, inflammation, and fever, cause gastric mucosal damage, including ulcers, directly or indirectly, by which the development of GI-safer (-sparing) NSAIDs relates to unmet medical needs. This study aimed to document the preventive effects of walnut polyphenol extracts (WPEs) against NSAID-induced gastric damage along with the molecular mechanisms. RGM-1 gastric mucosal cells were administered with indomethacin, and the expressions of the inflammatory mediators between indomethacin alone or a combination with WPEs were compared. The expressions of the inflammatory mediators, including COX-1 and COX-2, prostaglandin E2, 15-hydroxyprostaglandin dehydrogenase (15-PGDH), and antioxidant capacity, were analyzed by Western blot analysis, RT-PCR, and ELISA, respectively. HO-1, Nrf-2, and keap1 were investigated. The in vivo animal models were followed with in vitro investigations. The NSAIDs increased the expression of COX-2 and decreased COX-1 and 15-PGDH, but the WPEs significantly attenuated the NSAID-induced COX-2 expression. Interestingly, the WPEs induced the expression of 15-PGDH. By using the deletion constructs of the 15-PGDH promoter, we found that c-Jun is the most essential determinant of the WPE-induced up-regulation of 15-PGDH expression. We confirmed that the knockdown of c-Jun abolished the ability of the WPEs to up-regulate the 15-PGDH expression. In addition, the WPEs significantly increased the HO-1 expression. The WPEs increased the nuclear translocation of Nrf2 by Keap-1 degradation, and silencing Nrf2 markedly reduced the WPE-induced HO-1 expression. We found that the WPE-induced HO-1 up-regulation was attenuated in the cells harboring the mutant Keap1, in which the cysteine 151 residue was replaced by serine. These in vitro findings were exactly validated in indomethacin-induced gastric rat models. Daily walnut intake can be a promising nutritional supplement providing potent anti-inflammatory, antioxidative, and mucosa-protective effects against NSAID-induced GI damage.
Full article
(This article belongs to the Special Issue Pharmacological Activities of Secondary Metabolites and Derivates of Medicinal Plants around the World)
Open AccessArticle
Cytological and Transcriptome Analyses Provide Insights into Persimmon Fruit Size Formation (Diospyros kaki Thunb.)
by
Huawei Li, Yu**g Suo, Hui Li, Peng Sun, Shuzhan Li, Deyi Yuan, Weijuan Han and Jianmin Fu
Int. J. Mol. Sci. 2024, 25(13), 7238; https://doi.org/10.3390/ijms25137238 (registering DOI) - 30 Jun 2024
Abstract
Persimmon (Diospyros kaki Thunb.) fruit size variation is abundant. Studying the size of the persimmon fruit is helpful in improving its economic value. At present, the regulatory mechanism of persimmon fruit size formation is still unclear. In this study, the mechanism of
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Persimmon (Diospyros kaki Thunb.) fruit size variation is abundant. Studying the size of the persimmon fruit is helpful in improving its economic value. At present, the regulatory mechanism of persimmon fruit size formation is still unclear. In this study, the mechanism of fruit size formation was investigated through morphological, cytological and transcriptomic analyses, as well as exogenous ethrel and aminoethoxyinylglycine (AVG: ethylene inhibitor) experiments using the large fruit and small fruit of ‘Yaoxianwuhua’. The results showed that stages 3–4 (June 11–June 25) are the crucial morphological period for differentiation of large fruit and small fruit in persimmon. At this crucial morphological period, the cell number in large fruit was significantly more than that in small fruit, indicating that the difference in cell number is the main reason for the differentiation of persimmon fruit size. The difference in cell number was caused by cell division. CNR1, ANT, LAC17 and EB1C, associated with cell division, may be involved in regulating persimmon fruit size. Exogenous ethrel resulted in a decrease in fruit weight, and AVG treatment had the opposite effect. In addition, LAC17 and ERF114 were upregulated after ethrel treatment. These results indicated that high ethylene levels can reduce persimmon fruit size, possibly by inhibiting cell division. This study provides valuable information for understanding the regulation mechanism of persimmon fruit size and lays a foundation for subsequent breeding and artificial regulation of fruit size.
Full article
(This article belongs to the Special Issue Molecular Genetics and Plant Breeding 4.0)
Open AccessArticle
ProPept-MT: A Multi-Task Learning Model for Peptide Feature Prediction
by
Guoqiang He, Qingzu He, **yan Cheng, Rongwen Yu, Jianwei Shuai and Yi Cao
Int. J. Mol. Sci. 2024, 25(13), 7237; https://doi.org/10.3390/ijms25137237 (registering DOI) - 30 Jun 2024
Abstract
In the realm of quantitative proteomics, data-independent acquisition (DIA) has emerged as a promising approach, offering enhanced reproducibility and quantitative accuracy compared to traditional data-dependent acquisition (DDA) methods. However, the analysis of DIA data is currently hindered by its reliance on project-specific spectral
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In the realm of quantitative proteomics, data-independent acquisition (DIA) has emerged as a promising approach, offering enhanced reproducibility and quantitative accuracy compared to traditional data-dependent acquisition (DDA) methods. However, the analysis of DIA data is currently hindered by its reliance on project-specific spectral libraries derived from DDA analyses, which not only limits proteome coverage but also proves to be a time-intensive process. To overcome these challenges, we propose ProPept-MT, a novel deep learning-based multi-task prediction model designed to accurately forecast key features such as retention time (RT), ion intensity, and ion mobility (IM). Leveraging advanced techniques such as multi-head attention and BiLSTM for feature extraction, coupled with Nash-MTL for gradient coordination, ProPept-MT demonstrates superior prediction performance. Integrating ion mobility alongside RT, mass-to-charge ratio (m/z), and ion intensity forms 4D proteomics. Then, we outline a comprehensive workflow tailored for 4D DIA proteomics research, integrating the use of 4D in silico libraries predicted by ProPept-MT. Evaluation on a benchmark dataset showcases ProPept-MT’s exceptional predictive capabilities, with impressive results including a 99.9% Pearson correlation coefficient (PCC) for RT prediction, a median dot product (DP) of 96.0% for fragment ion intensity prediction, and a 99.3% PCC for IM prediction on the test set. Notably, ProPept-MT manifests efficacy in predicting both unmodified and phosphorylated peptides, underscoring its potential as a valuable tool for constructing high-quality 4D DIA in silico libraries.
Full article
(This article belongs to the Special Issue Proteomics and Its Applications in Disease 3.0)
Open AccessArticle
Exosomes Derived from Hypertrophic Scar Fibroblasts Suppress Melanogenesis in Normal Human Epidermal Melanocytes
by
Hui Song Cui, So Young Joo, Yoon Soo Cho, You Ra Lee, Yu Mi Ro, In Suk Kwak, Gi Yeun Hur and Cheong Hoon Seo
Int. J. Mol. Sci. 2024, 25(13), 7236; https://doi.org/10.3390/ijms25137236 (registering DOI) - 30 Jun 2024
Abstract
Post-burn hypertrophic scars often exhibit abnormal pigmentation. Exosomes play important roles in maintaining normal physiological homeostasis and in the pathological development of diseases. This study investigated the effects of the exosomes derived from hypertrophic scar fibroblasts (HTSFs) on melanocytes, which are pigment-producing cells.
[...] Read more.
Post-burn hypertrophic scars often exhibit abnormal pigmentation. Exosomes play important roles in maintaining normal physiological homeostasis and in the pathological development of diseases. This study investigated the effects of the exosomes derived from hypertrophic scar fibroblasts (HTSFs) on melanocytes, which are pigment-producing cells. Normal fibroblasts (NFs) and HTSFs were isolated and cultured from normal skin and hypertrophic scar (HTS) tissue. Both the NF- and HTSF-exosomes were isolated from a cell culture medium and purified using a column-based technique. The normal human epidermal melanocytes were treated with both exosomes at a concentration of 100 μg/mL at different times. The cell proliferation, melanin content in the medium, apoptotic factors, transcription factors, melanin synthesis enzymes, signaling, signal transduction pathways, and activators of transcription factors (STAT) 1, 3, 5, and 6 were investigated. Compared with the Dulbecco’s phosphate-buffered saline (DPBS)-treated controls and NF-exosomes, the HTSF-exosomes decreased the melanocyte proliferation and melanin secretion. The molecular patterns of apoptosis, proliferation, melanin synthesis, Smad and non-Smad signaling, and STATs were altered by the treatment with the HTSF-exosomes. No significant differences were observed between the DPBS-treated control and NF-exosome-treated cells. HTSF-derived exosomes may play a role in the pathological epidermal hypopigmentation observed in patients with HTS.
Full article
(This article belongs to the Section Molecular Biology)
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