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PURPOSE: To investigate the role of angiotensin II (Ang II) receptor subtypes in subconjunctival injury. METHODS: A wound-healing model was developed by subconjunctival blunt dissection in male wild-type, AT1a receptor-deficient (AT1a KO) and AT2 receptor-deficient (AT2 KO) mice. Collagen deposition and cell infiltration were evaluated histologically. Expression of collagen, matrix metalloproteinase (MMP), and tissue inhibitor of metalloproteinase-1 (TIMP-1) were determined by real-time PCR. RESULTS: Subconjunctival injury increased the infiltration of inflammatory cells, collagen deposition in the subconjunctival space, and the expression of collagen type I and type III, TIMP-1 and MMP2. In AT1a KO mice, collagen deposition, cell infiltration, and expression of collagen and TIMP-1 were inhibited, but MMP2 expression was enhanced. In contrast, in AT2 KO mice, the increase in collagen deposition, cell infiltration, and expression of collagen and TIMP-1 were further enhanced. CONCLUSIONS: These results indicate that AT1a and AT2 receptor stimulation may in addition to other mechanisms be antagonistically involved in the wound-healing process after subconjunctival injury.
Dr. S. Mizoue, Department of Molecular and Cellular Biology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Ehime, Japan
12.8.10 Woundhealing antifibrosis (Part of: 12 Surgical treatment > 12.8 Filtering surgery)