The Influence of Alloxan-Induced Diabetes on Müller Cell Contraction-Promoting Activities in Vitreous

摘要: Proliferative diabetic retinopathy (PDR) is a late-stage complication of diabetes in which fibrovascular tissues emerging from the retina exert tractional forces that can cause retinal detachment.1,2 There considerable interest identifying causal cells and stimuli driving their pathogenic responses because ability to arrest or attenuate any these processes would represent significant gain control this complication. Immunohistochemical studies epiretinal have identified number different cell types, including glia, immune cells, pigment epithelial fibroblast-like uncertain origin.3–8 Abundant circumstantial evidence indicates Muller are source detachment PDR. principal consistently scar tissue,3,6,8,9 laboratory revealed also derived phenotypically altered cells.9–11 Although normal lack capacity generate forces, not case with cells.11,12 Systematic study force generation vitro activity constitutive for fibroblast phenotype but stimulated by exogenous growth factors, members insulin-like factor (IGF) platelet-derived (PDGF) families.11,12 One findings particularly relevant examined changes contraction-promoting vitreous. It was determined vitreous contains little no stimulatory activity, it increased PDR.13 Studies factor-neutralizing antibodies attributed biological IGFs rather than PDGF, IGF did correlate hemorrhage as diagnostic feature, suggesting factors originate local production enter fluid through another mechanism. Finally, perhaps greatest interest, detected fluids eyes without PDR, change precede onset clinically proliferative disease. That temporally disease suggestive relationship worthy additional study. Unfortunately, limited availability samples patients early states precludes systematic humans. For biochemically oriented study, we made use an established large animal model hyperglycemia,14,15 goal evaluate temporal exists between increases