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Am J Physiol Gastrointest Liver Physiol 276: G1345-G1355, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 6, G1345-G1355, June 1999

Activation of VEGF and Ras genes in gastric mucosa during angiogenic response to ethanol injury

Michael K. Jones1, Rabiha M. Itani1, Hongtao Wang2, Morimasa Tomikawa2, I. James Sarfeh3, Sandor Szabo4, and Andrzej S. Tarnawski1,2,5

Departments of 5 Medicine, 3 Surgery, and 4 Pathology, 1 Veterans Affairs Medical Center, Long Beach, 90822; and 2 University of California, Irvine, California 92697

Our previous studies demonstrated that ethanol injury triggers the angiogenic response in gastric mucosa bordering necrosis. The present study was aimed to determine whether vascular endothelial growth factor (VEGF) (a potent angiogenic peptide selectively acting on endothelial cells) and Ras (a mediator of cell proliferation and a putative regulator of VEGF expression) are involved in gastric angiogenesis after ethanol injury. We studied the angiogenic response and expression of VEGF and Ras in gastric mucosa after ethanol injury. Ethanol damage triggered 1) angiogenesis in the gastric mucosa bordering necrosis, 2) significant increases in VEGF mRNA and protein expression, and 3) significant increases in the expression of Ki-ras mRNA and Ras proteins. Neutralizing anti-VEGF antibody significantly reduced (by greater than threefold) the angiogenic response to ethanol-induced injury. Moreover, mevastatin, an inhibitor of Ras activation, completely blocked the induction of VEGF expression in cultured primary endothelial cells. Because, in other tissues, VEGF is one of the most potent angiogenic factors and VEGF expression is dependent on Ras, our data indicate that Ras and VEGF are involved in gastric mucosal angiogenesis after ethanol injury.

ethanol; oncogenes; neutralizing antibody; competitive reverse transcriptase-polymerase chain reaction; inhibitor; vascular endothelial growth factor


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