Heparin-binding EGF-like growth factor (HB-EGF) promotes cell migration and adhesion via focal adhesion kinase.
Heparin-binding EGF-like growth factor (HB-EGF) promotes cell migration and adhesion via focal adhesion kinase.
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DOI：
10.1016/j.jss.2014.02.055
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发表时间：
2014-06-15
影响因子：
2.2
通讯作者：
Besner, Gail E.
中科院分区：
文献类型：
--
作者：
Su, Yanwei;Besner, Gail E.
细胞迁移和黏附在肠上皮损伤愈合和恢复中起着至关重要的作用。粘着斑激酶(FAK)在细胞-细胞外基质(ECM)信号转导中起重要作用。我们之前已经证明，肝素结合的表皮生长因子样生长因子(HB-EGF)在体外可以促进肠上皮细胞(IEC)的迁移和黏附。本研究旨在确定FAK是否参与HB-EGF诱导的IEC迁移和黏附。采用大鼠肠上皮细胞(RIE-1细胞)刮伤愈合模型，观察HB-EGF对依赖FAK的细胞迁移的影响。免疫荧光和免疫印迹法检测HB-EGF对磷酸化FAK(p-FAK)表达的影响。细胞黏附实验检测FAK在HB-EGF诱导的细胞与纤维连接蛋白(FN)黏附中的作用。HB-EGF显著促进擦伤后的愈合，这种作用在FAK抑制剂(FAK I-14)存在时被逆转(两者均与p<；0.05)。HB-EGF促进RIE-1细胞中p-FAK的表达，并诱导p-FAK重新分布和肌动蛋白重组。HB-EGF显著增加细胞在FN上的黏附和铺展(p<；0.05)。FAK I-14显著抑制内源性和HB-EGF诱导的细胞在FN上的黏附和扩散(P均<0.05)。FAK的磷酸化及其介导的信号转导在HB-EGF介导的IEC迁移和黏附中起重要作用。
Cell migration and adhesion are essential in intestinal epithelial wound healing and recovery from injury. Focal adhesion kinase (FAK) plays an important role in cell-extra cellular matrix (ECM) signal transduction. We have previously shown that heparin-binding epidermal growth factor-like growth factor (HB-EGF) promotes intestinal epithelial cell (IEC) migration and adhesion in vitro. The current study was designed to determine whether FAK is involved in HB-EGF-induced IEC migration and adhesion. A scrape wound healing model of rat intestinal epithelial cells (RIE-1 cells) was used to examine the effect of HB-EGF on FAK-dependent cell migration in vitro. Immunofluorescence and Western blot analyses were performed to evaluate the effect of HB-EGF on the expression of phosphorylated FAK (p-FAK). Cell adhesion assays were performed to determine the role of FAK in HB-EGF-induced cell adhesion on fibronectin (FN). HB-EGF significantly increased healing after scrape wounding, an effect that was reversed in the presence of a FAK inhibitor (FAK I-14) (both with p<0.05). HB-EGF increased p-FAK expression, and induced p-FAK redistribution and actin reorganization in migrating RIE-1 cells. Cell adhesion and spreading on FN were significantly increased by HB-EGF (p<0.05). FAK I-14 significantly inhibited both intrinsic and HB-EGF-induced cell adhesion and spreading on FN (both with p<0.05). FAK phosphorylation and FAK-mediated signal transduction play essential roles in HB-EGF-mediated IEC migration and adhesion.
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DOI：
10.1016/j.jss.2010.06.036
发表时间：
2011-12
期刊：
The Journal of surgical research
影响因子：
--
作者：
Radulescu A;Zhang HY;Chen CL;Chen Y;Zhou Y;Yu X;Otabor I;Olson JK;Besner GE
通讯作者：
Besner GE
DOI：
10.1038/labinvest.2011.167
发表时间：
2012-03
期刊：
Laboratory investigation; a journal of technical methods and pathology
影响因子：
--
作者：
通讯作者：
--
影响因子：
4.8
作者：
Avraham, HK;Lee, TH;Avraham, S
通讯作者：
Avraham, S
DOI：
10.1152/ajpheart.00444.2008
发表时间：
2009-03-01
影响因子：
4.8
作者：
Manso, Ana Maria;Kang, Seok-Min;Ross, Robert S.
通讯作者：
Ross, Robert S.
影响因子：
4.4
作者：
Mehta, VB;Besner, GE
通讯作者：
Besner, GE