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Stretch-induced cell proliferation is mediated by FAK-MAPK pathway

机译：牵张诱导的细胞增殖由FAK-MAPK途径介导

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Previously we reported that a uni-axial cyclic stretch treatment of rat 3Y1 fibroblasts induced focal adhesion kinase (FAK) tyrosine phosphorylation followed by mitogen-activated protein kinase (MAPK) activation (Wang et al., 2001) [Wang, J.G., Mlyazu, M., Matsushita, E., Sokabe, M., Naruse, K., 2001. Uni-axial cyclic stretch induces focal adhesion kinase (FAK) tyrosine phosphorylation followed by mitogen-activated protein kinase (MAPK) activation. Biochem. Biophys. Res. Comm. 288, 356-361]. In the present study, we investigated whether stretchinduced MA13K activation leads to proliferation of fibroblasts. 3Y1 fibroblasts were subjected to a uni-axial cyclic stretch treatment (1 Hz, 120% in length) and the bromodeoxyuridine (BrdU) incorporation was measured to access cell proliferation. BrdU incorporation increased in a time-dependent manner and became significant within 6 hours. To investigate the involvement of FAK, we transiently expressed FAK mutants that lacked tyrosine phosphorylation site (s) (F397Y, F925Y, F397/925Y). Transient expression of wild-type FAK or mock vector did not inhibit the stretch-induced BrdU incorporation, however, the FAK mutants significantly blocked BrdU incorporation. Treatment of the cells with MAPK inhibitors, PD98059 or S13203580, blocked extracellular signal- regulated kinase (ERK) phosphorylation and p38 MAPK phosphorylation, respectively, and also blocked stretchinduced BrdU incorporation. These results suggest that the stretch-induced FAK activation followed by MAPK activation plays an important role in the stretch-induced proliferation of 3Y1 fibroblasts. (c) 2005 Elsevier Inc. All rights reserved.
机译：先前我们曾报道，对大鼠3Y1成纤维细胞进行单轴循环拉伸处理后会引起粘着斑激酶（FAK）酪氨酸磷酸化，然后激活丝裂原激活的蛋白激酶（MAPK）（Wang等，2001）[Wang，JG，Mlyazu， M.，Matsushita，E.，Sokabe，M.，Naruse，K.，2001。单轴循环拉伸诱导粘着斑激酶（FAK）酪氨酸磷酸化，随后促有丝分裂原活化的蛋白激酶（MAPK）活化。生化。生物物理学。 Res。通讯288，356-361]。在本研究中，我们调查了拉伸诱导的MA13K激活是否导致成纤维细胞增殖。对3Y1成纤维细胞进行单轴循环拉伸处理（1 Hz，长度为120％），并测量了溴脱氧尿苷（BrdU）的掺入以进入细胞增殖。 BrdU掺入量随时间增加，并在6小时内变得显着。为了调查FAK的参与，我们瞬时表达缺少酪氨酸磷酸化位点的FAK突变体（F397Y，F925Y，F397 / 925Y）。野生型FAK或模拟载体的瞬时表达不会抑制拉伸诱导的BrdU掺入，但是，FAK突变体显着阻止了BrdU掺入。用MAPK抑制剂PD98059或S13203580处理细胞分别阻断了细胞外信号调节激酶（ERK）的磷酸化和p38 MAPK的磷酸化，还阻断了拉伸诱导的BrdU掺入。这些结果表明，拉伸诱导的FAK激活继之以MAPK激活在拉伸诱导的3Y1成纤维细胞增殖中起重要作用。 （c）2005 Elsevier Inc.保留所有权利。

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