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首页> 外文期刊>Digestive Diseases and Sciences >Loading of Mechanical Pressure Activates Mitogen-Activated Protein Kinase and Early Immediate Gene in Intestinal Epithelial Cells
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Loading of Mechanical Pressure Activates Mitogen-Activated Protein Kinase and Early Immediate Gene in Intestinal Epithelial Cells

机译：机械压力的加载激活肠上皮细胞中的丝裂素活化的蛋白激酶和早期即时基因。

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摘要

Intestinal mucosa is continuously exposed to mechanical forces. We examined whether pressure loading activates mitogen-activated protein kinase (MAPK) and expression of early immediate genes in intestinal epithelial cells. Pressure was applied to IEC18 cells by helium gas in a culture flask and pressure-induced cell proliferation was examined. The expression of early immediate genes, MAPK activity, and activation of nuclear factor activator protein-1 (AP-1) were also examined. Pressures significantly promoted cell proliferation with peak effect at 80 mm Hg. Pretreatment with either a protein kinase C inhibitor or tyrosine kinase inhibitors, but not calcium chelating agents significantly inhibited cell proliferation promoted by pressure. Early inductions of c-myc and c-fos proteins, increased activity of MAPK, and activation of AP-1 were observed by pressure loading. Our study showed that intestinal mucosal cell proliferation is promoted by mechanical pressure and various intracellular signaling pathways are involved in the process.
机译：肠粘膜持续受到机械力的作用。我们检查了压力加载是否激活了有丝分裂原激活的蛋白激酶（MAPK）和肠上皮细胞中早期即时基因的表达。在培养瓶中通过氦气对IEC18细胞施加压力，并检查压力诱导的细胞增殖。还检查了早期即时基因的表达，MAPK活性和核因子激活蛋白1（AP-1）的激活。压力显着促进细胞增殖，在80 mm Hg时达到峰值。用蛋白激酶C抑制剂或酪氨酸激酶抑制剂（而不是钙螯合剂）进行预处理可显着抑制压力促进的细胞增殖。通过压力加载观察到c-myc和c-fos蛋白的早期诱导，MAPK活性增加和AP-1激活。我们的研究表明，肠粘膜细胞的增殖是由机械压力促进的，并且各种细胞内信号通路都参与了该过程。

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