1. [The role of Src-tyrosine kinases in increasing vascular permeability during experimental ulcerative colitis].
- Author
-
Tolstanova HM, Khomenko TA, Ostapchenko LI, Szabo S, and Sandor Z
- Subjects
- Animals, Antigens, CD metabolism, Arrestins metabolism, Cadherins metabolism, Colitis, Ulcerative physiopathology, Colon blood supply, Colon enzymology, Colon metabolism, Disease Models, Animal, Endothelium, Vascular enzymology, Endothelium, Vascular metabolism, Intestinal Mucosa blood supply, Intestinal Mucosa enzymology, Intestinal Mucosa metabolism, Male, Rats, Rats, Sprague-Dawley, Vascular Endothelial Growth Factor Receptor-2 biosynthesis, beta-Arrestins, src-Family Kinases biosynthesis, Capillary Permeability physiology, Colitis, Ulcerative enzymology, src-Family Kinases physiology
- Abstract
We have shown the increase of Src(Tyr416) 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) (P < or = 0.001) and pSrc(Tyr416) 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 beta-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.
- Published
- 2010