李菲 1 , 陈长征 1 , 周俊 2 , 范雯 3 , 邢怡桥 4
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Objective To observe the expression of vascular endothelial growth factor A (VEGFA) and its receptors sFlt-1, kinase insert domain receptor (KDR) in lightinjured human retinal pigment epithelial (RPE) cells. Methods Cultured human RPE cells (8th - 12th generations) were divided into normal control group and light damage group. The cells of two groups were exposed to the 18 W cold white light (2200±300) Lux for 12 hours to induce light damage responses, but the cells of normal control group were packed by tinfoil with doubledeck high pressure disinfection. The VEGF-A, sFlt-1 and KDR mRNA and protein expressions were detected by reverse transcriptionpolymerase chain reaction (RT-PCR) and Western blot at 0, 6, 12, 24 hours after light damage. Results The VEGF-A mRNA and protein expressions in light damage group were significantly increased at 6 hours, and reached its peak at 12 hours after light damage which obviously higher than that in normal group (t=2.74, 2.93; P<0.05), and then went down gradually. The sFlt-1 mRNA and protein expressions in light damage group reached its peak at 12 hours after light damage which obviously higher than that in normal group (t=4.32, P<0.01), but obviously lower than that in normal group at 24 hours after light damage (t=2.41, P<0.05). The KDR mRNA and protein expressions in light damage group were obviously higher than that in normal group at 24 hours after light damage (t=2.89, P<0.05),but there was no changes at 6, 12 hours after light damage (t=1.84, P>0.05). Conclusions At 6, 12 hours after light damage, the expressions of VEGF-A and sFlt-1 increases significantly and KDR expression is stable in lightinjured RPE cells. At 24 hours after light damage, the expression of VEGF-A and sFlt-1 decreases, but KDR expression increases in light-injured RPE cells.

Citation: 李菲,陈长征,周俊,范雯,邢怡桥. Expression of vascular endothelial growth factor A and its receptors in light-injured human retinal pigment epithelial cells. Chinese Journal of Ocular Fundus Diseases, 2012, 28(2): 159-162. doi: Copy