血管内皮生长因子
发病机制
血管内皮生长因子A
细胞生长
转染
细胞骨架
生物
细胞生物学
生长因子
内皮干细胞
内分泌学
癌症研究
内科学
细胞
分子生物学
化学
细胞培养
医学
免疫学
生物化学
体外
受体
血管内皮生长因子受体
遗传学
作者
Xiangting Chen,Jie Xie,Ying Cui,Liang Zhang,Honghua Yu,Jing Chen,Mengxia He,Shuangxin Liu,Tian Huang,Lü Chen,Dong Fang,Ying Zhu,Shaochong Zhang,Qianli Meng
标识
DOI:10.1016/j.mce.2021.111378
摘要
We previously found the mutation frequency of cytoskeleton-associated protein 2 (CKAP2) was significantly increased in proliferative diabetic retinopathy (PDR) patients through whole exome sequencing. The present study was conducted to explore the expression and possible mechanism of CKAP2 in PDR patients and human retinal capillary endothelial cells (HRCECs) under high-glucose (HG) conditions.Expression of CKAP2 and p53 in the vitreous fluid and fibrovascular membrane (FVM) of PDR patients and HRCECs under HG conditions was observed. Cell proliferation, migration and tubule formation were assessed. Ranibizumab and siRNA transfection were used in the inhibition assay.CKAP2 and p53 were significantly increased in the ocular tissues of PDR patients. HG combined with VEGF treatment significantly up-regulated expression of CKAP2 and p53 in HRCECs. Inhibition of CKAP2 attenuated the abilities of cell proliferation, migration and tube formation under HG conditions. Blocking VEGF or p53 significantly decreased CKAP2 expression, whereas inhibition of CKAP2 failed to alter the level of VEGF or p53.CKAP2 is involved in the pathogenesis of PDR and regulated by VEGF and p53 under HG conditions.
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