ArticleArteriosclerosis, thrombosis, and vascular biology2013
Estrogen receptor-mediated regulation of microRNA inhibits proliferation of vascular smooth muscle cells.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 55 citations in OpenAlex.
- Clinical role and mechanism of miR-4443 in coronary heart disease: a prognostic marker and regulator of vascular smooth muscle cell Function.Journal of cardiothoracic surgery · 2026Article
- miR-203 Alleviates Myocardial Damage Caused by Acute Coronary Syndrome by Inhibiting CA125.Biochemical genetics · 2026Article
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- MicroRNAs regulate the vicious cycle of vascular calcification-osteoporosis in postmenopausal women.Molecular biology reports · 2024Review
- Modulation of Vascular Smooth Muscle Cell Multiplication, Apoptosis, and Inflammatory Damage by miR-21 in Coronary Heart Disease.Computational and mathematical methods in medicine · 2021Article
- MiR-203 regulates estrogen receptor α and cartilage degradation in IL-1β-stimulated chondrocytes.Journal of bone and mineral metabolism · 2020Article
- Cardiomyopathy Associated with Diabetes: The Central Role of the Cardiomyocyte.International journal of molecular sciences · 2019Review
- miRNA as a New Regulatory Mechanism of Estrogen Vascular Action.International journal of molecular sciences · 2018Review
- Role of miRNA in the Regulatory Mechanisms of Estrogens in Cardiovascular Ageing.Oxidative medicine and cellular longevity · 2018Review
- Diabetic Cardiomyopathy: Impact of Biological Sex on Disease Development and Molecular Signatures.Frontiers in physiology · 2018Review
- Anti-miR-203 suppresses ER-positive breast cancer growth and stemness by targeting SOCS3.Oncotarget · 2016Review
- Regulation of Vascular Smooth Muscle Cell Dysfunction Under Diabetic Conditions by miR-504.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- An overview of potential molecular mechanisms involved in VSMC phenotypic modulation.Histochemistry and cell biology · 2016Review
- Atherosclerosis and Vascular Biologic Responses to Estrogens: Histologic, Immunohistochemical, Biochemical, and Molecular Methods.Methods in molecular biology (Clifton, N.J.) · 2016Article
- GPR30 decreases with vascular aging and promotes vascular smooth muscle cells maintaining differentiated phenotype and suppressing migration via activation of ERK1/2.OncoTargets and therapy · 2016Article
- miRNAs regulated by estrogens, tamoxifen, and endocrine disruptors and their downstream gene targets.Molecular and cellular endocrinology · 2015Review
- MicroRNA-23a participates in estrogen deficiency induced gap junction remodeling of rats by targeting GJA1.International journal of biological sciences · 2015Article
- miR-599 Inhibits Vascular Smooth Muscle Cells Proliferation and Migration by Targeting TGFB2.PloS one · 2015Article
- Oestrogen signalling in white adipose progenitor cells inhibits differentiation into brown adipose and smooth muscle cells.Nature communications · 2014Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveEstradiol (E2) regulates gene transcription by activating estrogen receptor-α and estrogen receptor-β. Many of the genes regulated by E2 via estrogen receptors are repressed, yet the molecular mechanisms that mediate E2-induced gene repression are currently unknown. We hypothesized that E2, acting through estrogen receptors, regulates expression of microRNAs (miRs) leading to repression of expression of specific target genes. METHODS AND
resultsHere, we report that E2 significantly upregulates the expression of 26 miRs and downregulates the expression of 6 miRs in mouse aorta. E2-mediated upregulation of one of these miRs, miR-203, was chosen for further study. In cultured vascular smooth muscle cells (VSMC), E2-mediated upregulation of miR-203 is mediated by estrogen receptor-α (but not estrogen receptor-β) via transcriptional upregulation of the primary miR. We demonstrate that the transcription factors Zeb-1 and AP-1 play critical roles in mediating E2-induced upregulation of miR-203 transcription. We show further that miR-203 mediates E2-induced repression of Abl1, and p63 protein abundance in VSMC. Finally, knocking-down miR-203 abolishes E2-mediated inhibition of VSMC proliferation, and overexpression of miR-203 inhibits cultured VSMC proliferation, but not vascular endothelial cell proliferation.
conclusionsOur findings demonstrate that E2 regulates expression of miRs in the vasculature and support the estrogen receptors-dependent induction of miRs as a mechanism for E2-mediated gene repression. Furthermore, our findings demonstrate that miR-203 contributes to E2-induced inhibition of VSMC proliferation and highlight the potential of miR-203 as a therapeutic agent in the treatment of proliferative cardiovascular diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.