ArticleBMC molecular biology2019
MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.
Article in BMC molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- The role of plasma exosomal lnc-SNAPC5-3:4 in monitoring the efficacy of anlotinib in the treatment of advanced non-small cell lung cancer.Journal of cancer research and clinical oncology · 2022Trial
- Dual mechanism of human ATG10S in suppressing MEF2A-Driven pro-inflammatory responses.Autophagy · 2026Article
- Conserved signaling pathways and transcriptional regulators drive ovarian aging across species.Poultry science · 2026Article
- A spatial multi-omics atlas of immunosenescence reveals germinal-center B cell dysfunction in human lymph nodes.Cell press blue · 2026Article
- Multiomic profiling of responses to clinical and novel bisphosphonates reveals extraskeletal effects on ageing related signatures.Signal transduction and targeted therapy · 2026Article
- Sinomenine protects against oxidized low-density lipoprotein-induced human umbilical vein endothelial cell injury through regulating the myocyte enhancer factor 2 A/C-X-C motif chemokine ligand 14 pathway.Journal of bioenergetics and biomembranes · 2026Article
- Roles of insulin-like growth factor 1 receptor in growth regulation in 15q26 deletion and duplication syndrome.Biomedical reports · 2026Article
- Nephron-associated Support Cell Transcriptional Plasticity Expands in Hypertension.bioRxiv : the preprint server for biology · 2026Article
- Deletion of Circadian Rhythms Gene BMAL1 Impairs the Intestinal Epithelial Barrier and Exacerbates Intestinal Inflammation by Inducing Pyroptosis.Mediators of inflammation · 2026Article
- Article
- Myocyte enhancer factor 2A orchestrates vascular redox homeostasis via direct transcriptional activation of SIRT1.Acta biochimica et biophysica Sinica · 2025Article
- Transcriptome Profiling Based at Different Time Points after Hatching Deepened Our Understanding on Larval Growth and Development ofMetabolites · 2023Article
- Exosomes with overexpressed miR 147a suppress angiogenesis and infammatory injury in an experimental model of atopic dermatitis.Scientific reports · 2023Article
- Myocyte Enhancer Factor 2A Plays a Central Role in the Regulatory Networks of Cellular Physiopathology.Aging and disease · 2023Review
- Exploration of Hub Genes in Retinopathy of Prematurity Based on Bioinformatics Analysis of the Oxygen-Induced Retinopathy Model.Journal of ophthalmology · 2022Article
- Changes of Gene Expression Patterns of Muscle Pathophysiology-Related Transcription Factors During Denervated Muscle Atrophy.Frontiers in physiology · 2022Article
- Involvement of myocyte enhancer factor 2c in the pathogenesis of autism spectrum disorder.Heliyon · 2021Review
- MEF2A Is the Trigger of Resveratrol Exerting Protection on Vascular Endothelial Cell.Frontiers in cardiovascular medicine · 2021Article
- Identification and genomic analysis of pedigrees with exceptional longevity identifies candidate rare variants.Neurobiology of disease · 2020Article
- Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocyte enhancer factor 2A (MEF2A) plays an important role in cell proliferation, differentiation and survival. Functional deletion or mutation in MEF2A predisposes individuals to cardiovascular disease mainly caused by vascular endothelial dysfunction. However, the effect of the inhibition of MEF2A expression on human coronary artery endothelial cells (HCAECs) is unclear. In this study, expression of MEF2A was inhibited by specific small interference RNA (siRNA), and changes in mRNA profiles in response to MEF2A knockdown were analyzed using an Agilent human mRNA array.
resultsSilencing of MEF2A in HCAECs accelerated cell senescence and suppressed cell proliferation. Microarray analysis identified 962 differentially expressed genes (DEGs) between the MEF2A knockdown group and the negative control group. Annotation clustering analysis showed that the DEGs were preferentially enriched in gene ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways related to proliferation, development, survival, and inflammation. Furthermore, 61 of the 578 downregulated DEGs have at least one potential MEF2A binding site in the proximal promoter and were mostly enriched in the GO terms "reproduction" and "cardiovascular." The protein-protein interaction network analyzed for the downregulated DEGs and the DEGs in the GO terms "cardiovascular" and "aging" revealed that PIK3CG, IL1B, IL8, and PRKCB were included in hot nodes, and the regulation of the longevity-associated gene PIK3CG by MEF2A has been verified at the protein level, suggesting that PIK3CG might play a key role in MEF2A knockdown induced HCAEC senescence.
conclusionsMEF2A knockdown accelerates HCAEC senescence, and the underlying molecular mechanism may be involved in down-regulation of the genes related with cell proliferation, development, inflammation and survival, in which PIK3CG may play a key role.
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