ArticleCirculation research2015
MicroRNA miR145 regulates TGFBR2 expression and matrix synthesis in vascular smooth muscle cells.
Article in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 83 citations in OpenAlex.
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- Identification of Proteins and MicroRNAs with Prognostic Value for Assisted Reproduction Technology Outcomes in Follicular Fluid of Women with Endometriosis: A Pilot Study.International journal of molecular sciences · 2025Article
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- Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- S-propargyl-cysteine promotes the stability of atherosclerotic plaque via maintaining vascular muscle contractile phenotype.Frontiers in cell and developmental biology · 2023Article
- New Insights into the Functions of MicroRNAs in Cardiac Fibrosis: From Mechanisms to Therapeutic Strategies.Genes · 2022Review
- Expression levels of miR-22, miR-30c, miR-145, and miR-519d and their possible associations with inflammatory markers among patients with coronary artery disease.ARYA atherosclerosis · 2022Article
- The Etiology and Molecular Mechanism Underlying Smooth Muscle Phenotype Switching in Intimal Hyperplasia of Vein Graft and the Regulatory Role of microRNAs.Frontiers in cardiovascular medicine · 2022Review
- N-n-Butyl haloperidol iodide ameliorates liver fibrosis and hepatic stellate cell activation in mice.Acta pharmacologica Sinica · 2022Article
- Arterial stiffness and cardiac dysfunction in Hutchinson-Gilford Progeria Syndrome corrected by inhibition of lysyl oxidase.Life science alliance · 2021Article
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- Cancer-A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism.Frontiers in physiology · 2021Review
- Generation of transgenic mice that conditionally express microRNA miR-145.Genesis (New York, N.Y. : 2000) · 2020Article
- TGF-β and WNT signaling pathways in cardiac fibrosis: non-coding RNAs come into focus.Cell communication and signaling : CCS · 2020Review
- miR-145 inhibits the proliferation and migration of vascular smooth muscle cells by regulating autophagy.Journal of cellular and molecular medicine · 2020Article
- microRNA-143-3p attenuated development of hepatic fibrosis in autoimmune hepatitis through regulation of TAK1 phosphorylation.Journal of cellular and molecular medicine · 2020Article
- Osthole Alleviates Neointimal Hyperplasia in Balloon-Induced Arterial Wall Injury by Suppressing Vascular Smooth Muscle Cell Proliferation and Downregulating Cyclin D1/CDK4 and Cyclin E1/CDK2 Expression.Frontiers in physiology · 2020Article
- Pivotal Role of TGF-β/Smad Signaling in Cardiac Fibrosis: Non-coding RNAs as Effectual Players.Frontiers in cardiovascular medicine · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
rationaleMicroRNA miR145 has been implicated in vascular smooth muscle cell differentiation, but its mechanisms of action and downstream targets have not been fully defined.
objectiveHere, we sought to explore and define the mechanisms of miR145 function in smooth muscle cells. METHODS AND
resultsUsing a combination of cell culture assays and in vivo mouse models to modulate miR145, we characterized its downstream actions on smooth muscle phenotypes. Our results show that the miR-143/145 gene cluster is induced in smooth muscle cells by coculture with endothelial cells. Endothelial cell-induced expression of miR-143/145 is augmented by Notch signaling and accordingly expression is reduced in Notch receptor-deficient cells. Screens to identify miR145-regulated genes revealed that the transforming growth factor (TGF)-β pathway has a significantly high number of putative target genes, and we show that TGFβ receptor II is a direct target of miR145. Extracellular matrix genes that are regulated by TGFβ receptor II were attenuated by miR145 overexpression, and miR145 mutant mice exhibit an increase in extracellular matrix synthesis. Furthermore, activation of TGFβ signaling via angiotensin II infusion revealed a pronounced fibrotic response in the absence of miR145.
conclusionsThese data demonstrate a specific role for miR145 in the regulation of matrix gene expression in smooth muscle cells and suggest that miR145 acts to suppress TGFβ-dependent extracellular matrix accumulation and fibrosis, while promoting TGFβ-induced smooth muscle cell differentiation. Our findings offer evidence to explain how TGFβ signaling exhibits distinct downstream actions via its regulation by a specific microRNA.
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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.