國家衛生研究院 NHRI:Item 3990099045/4324
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/4324


    Title: Estrogen augments shear stress-induced signaling and gene expression in osteoblast-like cells via estrogen receptor-mediated expression of beta(1)-integrin
    Authors: Yeh, CR;Chiu, JJ;Lee, CI;Lee, PL;Shih, YT;Sun, JS;Chien, S;Cheng, CK
    Contributors: Division of Medical Engineering Research
    Abstract: Estrogen and mechanical forces are positive regulators for osteoblast proliferation and bone formation. We investigated the synergistic effect of estrogen and flow-induced shear stress on signal transduction and gene expression in human osetoblast-like MG63 cells and primary osteoblasts (HOBs) using activations of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) and expressions of c-fos and cyclooxygenase-2 (I) as readouts. Estrogen (17 beta-estradiol, 10 nM) and shear stress (12 dyn/cm(2)) alone induced transient phosphorylations of ERK and p38 MAPK in MG63 cells. Pretreating MG63 cells with 17 beta-estradiol for 6 hours before shearing augmented these shear-induced MAPK phosphorylations. Western blot and flow cytometric analyses showed that treating MG63 cells with 17 beta-estradiol for 6 hrs induced their beta(1)-integrin expression. This estrogen-induction of beta(1)-integrin was inhibited by pretreating the cells with a specific antagonist of estrogen receptor ICI 182,780. Both 17 beta-estradiol and shear stress alone induced c-fos and Cox-2 gene expressions in MG63 cells. Pretreating MG63 cells with 17 beta-estradiol for 6 hrs augmented the shear-induced c-fos and Cox-2 expressions. The augmented effects of 17 beta-estradiol on shear-induced MAPK phosphorylations and c-fos and Cox-2 expressions were inhibited by pretreating the cells with ICI 182,780 or transfecting the cells with beta(1)-specific small interfering RNA. Similar results on the augmented effect of estrogen on shear-induced signaling and gene expression were obtained with HOBs. Our findings provide insights into the mechanism by which estrogen augments shear stress responsiveness of signal transduction and gene expression in bone cells via estrogen receptor-mediated increases in beta(1)-integrin expression.
    Date: 2010-03
    Relation: Journal of Bone and Mineral Research. 2010 Mar;25(3):627-639.
    Link to: http://dx.doi.org/10.1359/jbmr.091008
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0884-0431&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000276767700024
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77953464428
    Appears in Collections:[Jeng-Jiann Chiu] Periodical Articles

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