G. M. Tolstanova1,2, T. A. Khomenko1, L.I.?Ostapchenko2, S. Szabo1, Zs. Sandor1
1University of California-Irvine, Long Beach, CA, USA,
2Taras Shevchenko Kyiv National University, Ukraine;
We have shown the increase of SrcTyr416 phosphorylation in rat colonic mucosa at early stages of 6% iodoacetamide-induced ulcerative colitis (UC), while the level of Src protein expression was not changed. Pretreatment of rats with Src inhibitor PP1 (0.2 mg/100 g, subcutaneously) decreased the colonic vascular permeability (VP) (Р ? 0.001) and pSrcTyr416 level during iodoacetamide-UC. Iodoacetamide-induced autophosphorylation and upregulation of VEGFR-2 was associated with Src activation in colonic mucosa of rats. Sequentially, protein-protein interaction between ?-arrestine2 and VE-cadherine was enhanced, that might be a reason of colonic endothelium barrier disruption. We concluded that Src plays a key role in the mechanisms of increasing the colonic VP during experimental UC.
Key words: iodoacetamide, Src-kinase, ulcerative colitis, vascular permeability, VEGF.
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