[The role of Src-tyrosine kinases in increasing vascular permeability during experimental ulcerative colitis].

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.

• Authors: H M Tolstanova, T A Khomenko, L I Ostapchenko, S Szabo, Z Sandor
• Journal: Ukrains'kyi biokhimichnyi zhurnal (1999 ) (Ukr Biokhim Zh (1999)) 2010 Jan-Feb Vol. 82 Issue 1 Pg. 117-22 Ukraine
• PMID: 20684236 (Publication Type: Journal Article)

Chemical References

• Antigens, CD
• Arrestins
• Cadherins
• beta-Arrestins
• cadherin 5
• Vascular Endothelial Growth Factor Receptor-2
• src-Family Kinases

Topics

• Animals
• Antigens, CD (metabolism)
• Arrestins (metabolism)
• Cadherins (metabolism)
• Capillary Permeability (physiology)
• Colitis, Ulcerative (enzymology, physiopathology)
• Colon (blood supply, enzymology, metabolism)
• Disease Models, Animal
• Endothelium, Vascular (enzymology, metabolism)
• Intestinal Mucosa (blood supply, enzymology, metabolism)
• Male
• Rats
• Rats, Sprague-Dawley
• Vascular Endothelial Growth Factor Receptor-2 (biosynthesis)
• beta-Arrestins
• src-Family Kinases (biosynthesis, physiology)