Purchase this article with an account.
Kristin Olsson, Christopher Talbot, James Kenneth Kubilus, Thomas Linsenmayer; Ultraviolet light (UV-B) induced apoptosis in human corneal epithelial cells. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5746.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Ultraviolet (UV) light is damaging to cells. Despite this, our previous studies using the chicken as a model system demonstrated that corneal epithelial cells are far more resistant to UV damage than other cell types. These studies suggest that corneal epithelial cells may possess unique UV-protective mechanisms. However, the mechanism of cell death in response to UV-B induced damage in human corneal epithelial cells is unclear. Here we investigated the effects of UV-B irradiation on telomerase-immortalized human corneal epithelial (hTCEpi) cells to examine these mechanisms.
hTCEpi cells were exposed to a series of dosages of UV-B irradiation. Protein isolates from exposed and unexposed cells were analyzed for pJNK, the form of JNK active in apoptosis, and compared through western blotting. Cell morphology of the different treatment groups was assessed by light microscopy. PCR array and western blot were used to determine the expression of apoptotic markers in the hTCEpi cells following UV-B exposure.
Western blotting showed an increase in pJNK with increasing UV-B dosage. Light microscopy showed that for dosages greater than 12.5 mJ/cm2, increased cell debris and vesicular nuclei were present, likely reflecting necrosis. PCR arrays showed increases in apoptotic factors such as BCL2L11, CD27, DAPK1, and decreases in factors such as APAF1 and BCL10.
hTCEpi cells undergo changes in the expression of programmed cell death related genes in response to UV-B. However, exposure to greater than 12.5 mJ/cm2 of UV-B led to cell necrosis that was likely due to the amount of cellular damage.
This PDF is available to Subscribers Only