Regulation of TGF-β-mediated endothelial-mesenchymal transition by microRNA-27.
Hiroshi I. Suzuki,Hiroshi I. Suzuki,Akihiro Katsura,Hajime Mihira,Masafumi Horie,Akira Saito,Kohei Miyazono +6 more
TLDR
It is reported that microRNA-27b positively regulates transforming growth factor-β (TGF-β)-induced EndMT of MS-1 mouse pancreatic microvascular endothelial cells, suggesting important roles of miR-27 in TGF- β-driven EndMT.Abstract:
Multiple microRNAs (miRNAs) regulate epithelial-mesenchymal transition and endothelial-mesenchymal transition (EndMT). Here we report that microRNA-27b (miR-27b) positively regulates transforming growth factor-β (TGF-β)-induced EndMT of MS-1 mouse pancreatic microvascular endothelial cells. TGF-β induced miR-23b/24-1/27b expression, and inhibition of miR-27 suppressed TGF-β-mediated induction of mesenchymal genes. Genome-wide miRNA target analysis revealed that miR-27 targets Elk1, which acts as a competitive inhibitor of myocardin-related transcription factor-serum response factor signalling and as a myogenic repressor. miR-27b was also found to regulate several semaphorin receptors including Neuropilin 2, Plexin A2 and Plexin D1. These results suggest important roles of miR-27 in TGF-β-driven EndMT.read more
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Journal ArticleDOI
Endothelial to Mesenchymal Transition in Cardiovascular Disease: JACC State-of-the-Art Review.
Jason C. Kovacic,Stefanie Dimmeler,Richard P. Harvey,Toren Finkel,Elena Aikawa,Guido Krenning,Andrew H. Baker +6 more
TL;DR: A framework for its systematic advancement at the molecular and translational levels is proposed and a number of challenges are reviewed, including the lack of a precise functional and molecular definition, lack of understanding of the causative pathological role of EndMT in CVDs, and a lack of robust human data corroborating the extent and causality.
Journal ArticleDOI
Endothelial to Mesenchymal Transition: Role in Physiology and in the Pathogenesis of Human Diseases.
TL;DR: The identification of molecules and regulatory pathways involved in EndMT and the discovery of specific EndMT inhibitors should provide novel therapeutic approaches for various human disorders mediated by EndMT.
Journal ArticleDOI
circHECTD1 promotes the silica-induced pulmonary endothelial-mesenchymal transition via HECTD1.
Shencun Fang,Shencun Fang,Huifang Guo,Yusi Cheng,Zewei Zhou,Wei Zhang,Bing Han,Wei Luo,Jing Wang,Weiping Xie,Jie Chao +10 more
TL;DR: SiO2-induced increases in cell proliferation, migration, and changes in marker levels were restored by either a small interfering RNA (siRNA) targeting circHectD1 or overexpression of HECTD1 via the CRISPR/Cas9 system, confirming the involvement of the circHECTD 1/HECTd1 pathway in the EndMT.
Journal ArticleDOI
Role of flow-sensitive microRNAs and long noncoding RNAs in vascular dysfunction and atherosclerosis.
TL;DR: The flow-sensitive lncRNA STEEL is discussed along with other lncRNAs studied in the context of vascular pathophysiology and atherosclerosis such as MALat1, MIAT1, ANRIL, MYOSLID, MEG3, SENCR, SMILR, LISPR1, and H19.
Journal ArticleDOI
MicroRNA Control of TGF-β Signaling
TL;DR: The connection between TGF-β signaling and the miRNA pathway is summarized, placing particular emphasis on the regulation of miRNA expression by TGF -β signaling, the modulation of TGF –β signaling by miRNAs, the mi RNA-mediated modulation of EMT and endothelial–mesenchymal transition as well as the crosstalk between miRNA and TGF–β pathways in the tumor microenvironment.
References
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