Berman M B
Department of Ophthalmology, University of Texas Southwestern Medical Center at Dallas 75235-9057.
Cornea. 1993 Sep;12(5):420-32. doi: 10.1097/00003226-199309000-00009.
Plasmin was found to degrade the fibronectin (Fn) mesh produced by cultures of normal rabbit corneal fibroblasts, cause breakdown of F-actin-containing microfilament bundles ("stress fibers"), and increase levels of active type I interstitial collagenase (MMP-1) in the medium. Fibroblast cultures derived from alkali-burned, ulcerating rabbit corneas also responded to plasmin by secreting collagenase, detected only in active form. Moreover, harvests from organ cultures of ulcerating corneas not only had higher levels of urokinase-like plasminogen activator (uPA) than normal cultures but also had higher levels of Fn degradation fragments. The results are consistent with reports that indicate that perturbation of the alpha 5 beta 1 integrin (Fn) receptor by proteolytic fragments of Fn causes the increased synthesis and secretion of MMP-1. The uPA/plasmin system, therefore, might have an important role in regulating collagenase synthesis, secretion, and activation during wound remodelling and stromal ulceration.
研究发现，纤溶酶可降解正常兔角膜成纤维细胞培养物产生的纤连蛋白（Fn）网，导致含F-肌动蛋白的微丝束（“应力纤维”）分解，并增加培养基中活性I型间质胶原酶（MMP-1）的水平。源自碱烧伤、溃疡兔角膜的成纤维细胞培养物也通过分泌胶原酶对纤溶酶产生反应，且仅以活性形式检测到。此外，溃疡角膜器官培养物的收获物不仅比正常培养物具有更高水平的尿激酶样纤溶酶原激活物（uPA），而且具有更高水平的Fn降解片段。这些结果与以下报道一致，即Fn的蛋白水解片段对α5β1整合素（Fn）受体的扰动会导致MMP-1合成和分泌增加。因此，uPA/纤溶酶系统可能在伤口重塑和基质溃疡过程中调节胶原酶的合成、分泌和激活方面发挥重要作用。
