Purchase this article with an account.
T. Li, U. Lu; Protective Effect of CCCTC Binding Factoron Stress-Induced Apoptosis in Corneal Cells. Invest. Ophthalmol. Vis. Sci. 2007;48(13):549.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Our previous study indicates that CTCF, a nuclear transcriptional factor, involves regulation of growth factor-induced gene regulation and cell proliferation. In the present study, we investigated the protective effect of CTCF on stress-induced apoptosis in human corneal epithelial (HCE) cells.
HCE cells were cultured in DMEM/F12 medium with 10% FBS and 5 µg/ml insulin. UV and hyperosmotic-induced cell death was evaluated by MTT assay, caspase-3 activation and PARP degradation. The cellular CTCF expressing Level was manipulated by transiently-transfecting pcDNA4-CTCF cDNA and CTCF specific SiRNA respectively.
We found that UV and hyper-osmotic stresses induced down-regulation of CTCF at both mRNA and protein levels in HCE cells. The stress-induced CTCF down-regulation was followed by significant caspase 3 activation, PARP degradation and decreases in cell viability, suggesting that CTCF is an anti-apoptotic factor and plays an important role in the signaling pathways of stress-induced apoptosis. Furthermore, the above hypothesis was verified by experiments in which cellular endogenous CTCF level was manipulated. Transient transfection of human CTCF markedly suppressed stress-induced apoptosis in HCE cells. In contrast, knocking down of CTCF mRNA using siRNA specific to CTCF significantly enhanced stress-induced apoptosis.
the present study reports for the first time that CTCF plays a significant anti-apoptotic role in regulation of stress-induced programmed cell death.
This PDF is available to Subscribers Only