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- W2021504025 abstract "Previous studies suggest the existence of two separate and distinct mechanisms of endothelial wound healing (i.e., cell migration and cell spreading), which may be controlled by unique, injury-dependent, wound-related factors. The purpose of our study was to evaluate potential biologic mediators regulating healing of the growth arrested cat endothelium by using an ex vivo, organ-culture model. Three buttons were punched from each cornea of 11 cats with a 6-mm trephine. A 1− to 2-mm diameter endothelial scrape injury (SI) was made, and buttons were cultured in (a) serum-free media (SFM), (b) serum plus media (20% fetal calf serum), (c) SFM plus basic fibroblast growth factor (bFGF), (d) SFM plus bFGF and heparin, (e) SFM plus transforming growth factor-β1 (TGFβ1), or (f) SFM plus TGFβ1 and anti-TGFβ1. At various times from 8–48 h after injury, buttons were stained with phalloidin and anti-ZO-1, and imaged by using laser scanning confocal microscopy. Evaluation of SI in cat corneal buttons under serum-free conditions showed maintenance of normal endothelial differentiation, indicating that the organ-culture SI model mimics in vivo SI. Addition of TGFβ1 produced a dramatic reorganization of apical F-actin and development of stress fibers, as well as the loss of normal cell border-associated ZO-1 distribution. The effects of TGFβ1 were blocked by the neutralizing antibodies to TGFβ1. Addition of serum or bFGF produced much less pronounced changes in F-actin and ZO-1 distribution. These results suggest that TGFp, may play a critical role in modulating the wound-healing response of the corneal endothelium." @default.
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- W2021504025 title "Effects of Basic FGF and TGF??1 on F-Actin and ZO-1 Organization During Cat Endothelial Wound Healing" @default.
- W2021504025 doi "https://doi.org/10.1097/00003226-199609000-00013" @default.
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