國家衛生研究院 NHRI:Item 3990099045/4076
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    题名: Loss of the serum response factor cofactor, cysteine-rich protein 1, attenuates neointima formation in the mouse
    作者: Lilly, B;Clark, KA;Yoshigi, M;Pronovost, S;Wu, ML;Periasamy, M;Chi, M;Paul, RJ;Yet, SF;Beckerle, MC
    贡献者: Institute of Cellular and Systems Medicine
    摘要: Background and Purpose-Cysteine-rich proteins (CRPs) 1 and 2 are cytoskeletal LIM-domain proteins thought to be critical for smooth muscle differentiation. Loss of murine CRP2 does not overtly affect smooth muscle differentiation or vascular function; it does exacerbate neointima formation in response to vascular injury. Because CRPs 1 and 2 are coexpressed in the vasculature, we hypothesize that CRPs 1 and 2 act redundantly in smooth muscle differentiation. METHODS AND RESULTS: We generated Csrp1 (gene name for CRP1) null mice by genetic ablation of the Csrp1 gene and found that mice lacking CRP1 are viable and fertile. Smooth muscle-containing tissues from Csrp1-null mice are morphologically indistinguishable from wild-type mice and have normal contractile properties. Mice lacking CRPs 1 and 2 are viable and fertile, ruling out functional redundancy between these 2 highly related proteins as a cause for the lack of an overt phenotype in the Csrp1-null mice. Csrp1-null mice challenged by wire-induced arterial injury display reduced neointima formation, opposite to that seen in Csrp2-null mice, whereas Csrp1/Csrp2 double-null mice produce a wild-type response. CONCLUSIONS: Smooth muscle CRPs are not essential for normal smooth muscle differentiation during development, but may act antagonistically to modulate the smooth muscle response to pathophysiological stress.
    日期: 2010-04
    關聯: Arteriosclerosis, Thrombosis, and Vascular Biology. 2010 Apr;30(4):694-701.
    Link to: http://dx.doi.org/10.1161/atvbaha.109.200741
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1079-5642&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000275712500012
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77950893076
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