Increase of Protein Tyrosine Phosphorylation in Rat Retina After Ischemia-Reperfusion Injury

作者: B M Koroma , E de Juan , K Imai , A Hayashi

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摘要: PURPOSE This study was conducted to examine the effect of retinal ischemia-reperfusion injury on protein tyrosine phosphorylation, production angiogenic growth factors, and activation signal proteins in kinase pathways. METHODS Ischemia-reperfusion induced rats by compression optic nerve for 2 hours. The were killed, retinas collected at 0, 1, 6, 24, 48, 96, or 168 hours reperfusion. Tyrosine phosphorylation retina examined Western blot analysis immunohistochemistry. Angiogenic factors their receptors, such as basic fibroblast factor (bFGF) Flg, vascular endothelial (VEGF) Flk-1, platelet-derived (PDGF)-B chain PDGF-beta receptor, five intracellular (phosphatidylinositol 3-kinase [PI3K], phospholipase C gamma [PLC gamma], C-Src, SHC, mitogen-activated [MAPK]) analysis. RESULTS Protein increased after injury, reaching a peak 48 Increased staining tyrosine-phosphorylated inner evident immunohistochemical examination. amount bFGF decreased but amounts VEGF PDGF-B increased. PLC gamma, MAPK reperfusion, receptor PI3K CONCLUSIONS rat leads pathway, increasing factors. resultant MAPK, PI3K, may play an important role ischemia-induced changes cell proliferation.

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