Loss of Fgf2 Retards Proliferation without Impairing Epithelial-mesenchymal Transition of Lens Epithelial Cells upon Injury

Abstract

Abstract: : Purpose:Use of FGF2-null mice to investigate injury-induced proliferation and epithelial-mesenchymal transition (EMT) of mouse lens epithelial cells (LECs).Methods:The animal protocol was approved by IACUC of University of Cincinnati, Wakayama Medical University. The procedure approved by National Cancer Institute/NIH was employed. The animals were anesthetized both systemically with pentobarbital sodium, i.p. and topically with oxybyprocaine eyedrop. An anterior lens capsular injury was created in one eye of individual animals with a hypodermic needle. Animals were sacrificed at Day 2, 5, and 10 days following a 2 hr-BrdU labeling. Paraffin sections were processed for immunostaining of BrdU, α-smooth muscle actin (α SMA) and type I collagen.Results:Histology with HE stain did not revealed difference in LEC morphology between Fgf2-/- (KO) and Fgf2+/+ (WT) mice. The number of BrdU-labeled cells in WT mouse lenses was approximately 50% higher than in KO mice throughout the healing intervals examined (statistically significant at Day 10). α SMA and collagen I were both negative in LECs at Day 2 post-injury both in KO and WT mice. The cells and matrix were positive for α SMA and collagen I, respectively, at Day 5 and 10 post-injury in KO and WT mice.Conclusions: Loss of FGF2 decreases the rate of injury-induced cell proliferation in the murine lens, but does not purturb the process of EMT.

Keywords: wound healing • proliferation • growth factors/growth factor receptors