Abstract

The ability of insulin and IGF-2 to support wound repair in the organ-cultured rat corneal endothelium was investigated. Corneas given a circular transcorneal freeze injury, were explanted into organ cultures containing either insulin or IGF-2 and cultured up to72 h. Both factors increased [³H]-thymidine incorporation and mitotic levels compared to controls. Insulin’s ability to mediate wound closure without serum was dependent on its continuous presence in the medium. PKC was also investigated in endothelial repair using the PKC promoter phorbol 12-myristate 13-acetate (PMA). Concentrations between 10⁻⁶ and 10⁻⁸ M, PMA failed to accelerate wound closure. When injured endothelia were cultured in the presence of insulin and the PKC inhibitor H-7, wound closure was also unaffected. These results indicate that insulin and IGF-2 stimulate cell growth in injured rat corneal endothelium and that insulin without the benefit of serum promotes wound closure in situ independent of the PKC pathway.

摘要

研究了胰岛素和 IGF-2 在器官培养的大鼠角膜内皮中支持伤口修复的能力。受到圆形经角膜冷冻损伤的角膜被移植到含有胰岛素或 IGF-2 的器官培养物中，并培养长达 72 小时。与对照相比，这两个因素都增加了[ ³ H]-胸苷掺入和有丝分裂水平。胰岛素在没有血清的情况下介导伤口闭合的能力取决于它在培养基中的持续存在。还使用 PKC 启动子佛波醇 12-肉豆蔻酸酯 13-乙酸 (PMA) 在内皮修复中研究了 PKC。浓度介于 10 ^-6和 10 ^{-8 之间}M，PMA 未能加速伤口闭合。当在胰岛素和 PKC 抑制剂 H-7 存在下培养受伤的内皮时，伤口闭合也不受影响。这些结果表明胰岛素和 IGF-2 会刺激受损大鼠角膜内皮细胞的生长，而不含血清的胰岛素可促进伤口原位闭合，而与 PKC 途径无关。