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学科主题: 基础医学
题名:
MicroRNA Mediation of Endothelial Inflammatory Response to Smooth Muscle Cells and Its Inhibition by Atheroprotective Shear Stress
作者: Chen, Li-Jing1; Chuang, Li1; Huang, Yi-Hsuan1; Zhou, Jing4; Lim, Seh Hong1; Lee, Chih-I1; Lin, Wei-Wen5; Lin, Ting-Er1; Wang, Wei-Li1; Chen, Linyi2; Chien, Shu6,7; Chiu, Jeng-Jiann1,3
关键词: atherosclerosis ; endothelial cell ; microRNA ; shear stress ; smooth muscle myocytes
刊名: CIRCULATION RESEARCH
发表日期: 2015-03-27
DOI: 10.1161/CIRCRESAHA.116.305987
卷: 116, 期:7, 页:1157-+
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems ; Hematology ; Peripheral Vascular Disease
研究领域[WOS]: Cardiovascular System & Cardiology ; Hematology
关键词[WOS]: NF-KAPPA-B ; PHENOTYPIC MODULATION ; DISTURBED FLOW ; EXPRESSION ; HYPERPLASIA ; ACTIVATION ; MECHANISMS ; INDUCTION ; MIR-146A ; TARGETS
英文摘要:

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: Coculturing ECs with sSMCs under static condition causes initial increases of 4 antiinflammatory 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 hours and those for miR-451/98 lasted for only 6 to 12 hours. Shear stress (12 dynes/cm(2)) to cocultured ECs for 24 hours augments these 4 miR expressions. In vivo, these 4 miRs are highly expressed in neointimal ECs in injured arteries under physiological levels of flow, but not expressed under flow stagnation. MiR-146a, miR-708, miR-451, and miR-98 target interleukin-1 receptor-associated kinase, inhibitor of nuclear factor-kappa B kinase subunit-gamma, interleukin-6 receptor, and conserved helix-loop-helix ubiquitous kinase, respectively, to inhibit nuclear factor-kappa B signaling, which exerts negative feedback control on the biogenesis of these miRs. Nuclear factor-E2-related factor (Nrf)-2 is critical for shear-induction of miR-146a in cocultured 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.

语种: 英语
所属项目编号: MOST-103-2321-B-400-001/MOST-103-2325-B-016-003 ; NSFC-81470590/BNSF-7152081 ; HL-106579/HL-108735
WOS记录号: WOS:000351834500016
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/64779
Appears in Collections:基础医学院_期刊论文

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作者单位: 1.Natl Hlth Res Inst, Inst Cellular & Syst Med, Miaoli 350, Taiwan
2.Natl Tsing Hua Univ, Inst Mol Med, Hsinchu, Taiwan
3.Natl Tsing Hua Univ, Inst Biomed Engn, Hsinchu, Taiwan
4.Peking Univ, Basic Med Coll, Dept Physiol & Pathophysiol, Beijing 100871, Peoples R China
5.Taichung Vet Gen Hosp, Dept Cardiol, Internal Med, Taichung, Taiwan
6.Univ Calif San Diego, Dept Bioengn, La Jolla, CA 92093 USA
7.Univ Calif San Diego, Inst Engn Med, La Jolla, CA 92093 USA

Recommended Citation:
Chen, Li-Jing,Chuang, Li,Huang, Yi-Hsuan,et al. MicroRNA Mediation of Endothelial Inflammatory Response to Smooth Muscle Cells and Its Inhibition by Atheroprotective Shear Stress[J]. CIRCULATION RESEARCH,2015,116(7):1157-+.
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