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Louis Zhang, Lixing W Reneker; Increase of Apoptosis in the Lenses of Foxe3 Mutant Mice. Invest. Ophthalmol. Vis. Sci. 2014;55(13):727.
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Mutations in human FOXE3 forkhead transcription factor are linked to congenital eye disease called Peters’ anomaly, which is characterized by central corneal opacity and lens-corneal adhesions. Programmed cell death (PCD or apoptosis) plays an essential role in separation of nascent lens vesicle from the overlaying surface ectoderm. In this study, we investigated whether loss of Foxe3 function had an effect on apoptosis during lens development.
Homozygous dysgenetic lens (dyl) mice, which are loss-of-function mutant of Foxe3, were used in the study. Apoptosis was detected by TUNEL assay. The expression of phosphorylated ERK (pERK), pAKT and survivin in wild type (WT) and dyl lenses was analyzed by immunostaining.
In E11.5 dyl lenses, apoptotic cells were detected in both anterior and posterior part of the lens vesicle, and the level was increased when compared to the WT lenses at the same age. Apoptosis was also found in E18.5 dyl but not WT lenses. These results suggest that Foxe3 is essential for lens cell survival in addition to its function in other cellular processes such as cell proliferation during lens development. It is known that expression of PDGF receptor alpha (PDGFRalpha) requires Foxe3 and the level of PDGFRalpha is significantly reduced in dyl lenses. To access whether increase of apoptosis in dyl lenses was due to reduction in growth factor receptor signaling activity, we examined the levels of pERK, pAKT and surviving in E18.5 lenses by immunostaining. We found no significant differences between the WT and dyl lenses.
In addition to its function in cell proliferation and differentiation, Foxe3 is also required for cell survival, particularly at the stage of lens vesicle development. Apoptosis in E18.5 dyl lenses is not due to the reduction of pERK, pAKT and surviving levels.
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