國家衛生研究院 NHRI:Item 3990099045/8508
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/8508


    Title: MicroRNA mediation of endothelial inflammatory response to smooth muscle cells and its inhibition by atheroprotective shear stress
    Authors: Chen, LJ;Chuang, L;Huang, YH;Zhou, J;Lim, SH;Lee, CI;Lin, WW;Lin, TE;Wang, WL;Chen, L;Chien, S;Chiu, JJ
    Contributors: Institute of Cellular and Systems Medicine
    Abstract: Rationale: In atherosclerotic lesions, synthetic smooth muscle cells (sSMCs) induce aberrant microRNA (miR) profiles in endothelial cells (ECs) under flow stagnation. Increase in shear stress induces favorable miR modulation to mitigate sSMC-induced inflammation. Objective: To address the role of miRs in sSMC-induced EC inflammation and its inhibition by shear stress. Methods and Results: Co-culturing ECs with sSMCs under static condition causes initial increases of four anti-inflammatory miRs (146a/708/451/98) in ECs followed by decreases below basal levels at 7 days; the increases for miR-146a/708 peaked at 24 h and those for miR-451/98 lasted for only 6-12 h. Shear stress (12 dynes/cm2) to co-cultured ECs for 24 h augments these four miR expressions. In vivo, these four miRs are highly expressed in neointimal ECs in injured arteries under physiological levels of flow, but not expressed under flow stagnation. MiR-146a, -708, -451, and -98 target interleukin (IL)-1 receptor-associated kinase, inhibitor of nuclear factor-kappaB (NF-kappaB) kinase subunit-gamma, IL-6 receptor, and conserved helix-loop-helix ubiquitous kinase, respectively, to inhibit NF-kappaB signaling, which exerts negative feedback control on the biogenesis of these miRs. NF-E2-related factor-2 (Nrf-2) is critical for shear-induction of miR-146a in co-cultured ECs. Silencing either Nrf-2 or miR-146a led to increased neointima formation of injured rat carotid artery under physiological levels of flow. Overexpressing miR-146a inhibits neointima formation of rat or mouse carotid artery induced by injury or flow cessation. Conclusions: Nrf-2-mediated miR-146a expression is augmented by atheroprotective shear stress in ECs adjacent to sSMCs to inhibit neointima formation of injured arteries.
    Date: 2015-03
    Relation: Circulation Research. 2015 Mar;116(7):1157-1169.
    Link to: http://dx.doi.org/10.1161/circresaha.116.305987
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0009-7330&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000351834500016
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84942980888
    Appears in Collections:[Jeng-Jiann Chiu ] Periodical Articles

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