Gao M-L, Deng W-L, Huang N, Wang Y-Y, Lei X-L, Xu Z-Q, Hu D-N, Cai J-Q, Lu F, Jin Z-B
Lab for Stem Cells and Retinal Regeneration, Division of Ophthalmic Genetics, Institute for Stem Cell Research, The Eye Hospital of Wenzhou Medical University, State Key Laboratory Cultivation Base and Key Laboratory of Vision Science, Ministry of Public Health , Wenzhou 325027, China.
Tissue Culture Center, New York Eye and Ear Infirmary, New York Medical College , Valhalla, 10595 New York, USA.
Cell Death Discov. 2016 Feb 29;2:16013. doi: 10.1038/cddiscovery.2016.13. eCollection 2016.
To better understand the molecular mechanisms responsible for light-induced damage in retinal pigmented epithelial (RPE) cells, we developed an automated device to recapitulate intense light exposure. When compared with human fibroblasts, ARPE-19 cells that had been exposed to blue-rich light-emitting diode-light of 10 000 Lux at 37 °C for 9 h displayed dramatic cellular apoptosis. Collectively, gene expression profiling and qPCR demonstrated that growth arrest and DNA damage-45α (GADD45α) expression was markedly upregulated. Transient knockdown of GADD45α partially attenuated light-damage-induced apoptosis in ARPE-19 cells, whereas GADD45α overexpression dramatically increased it. These results demonstrate the critical function of GADD45α in light-induced RPE cellular apoptosis. Quantitative reverse transcription-PCR and western blotting revealed that the upregulation of GADD45α was under direct control of p53. Moreover, treatment with Ly294002, an inhibitor of AKT phosphorylation, further promoted GADD45α gene transcription in both non-light and light-damaged ARPE-19 cells. Treatment also exacerbated RPE cellular apoptosis after light exposure, confirming that inhibition of Akt phosphorylation increases GADD45α expression. Collectively, our findings reveal that light irrigation induces human RPE cellular apoptosis through upregulation of GADD45α expression mediated through both the p53 and phosphatidylinositol 3-kinase-AKT signaling pathways. These results provide new insights into human retinal diseases elicited by light damage and open a new avenue for disease prevention and treatment.
为了更好地理解视网膜色素上皮(RPE)细胞中光诱导损伤的分子机制,我们开发了一种自动装置来模拟强光照射。与人类成纤维细胞相比,ARPE - 19细胞在37°C下暴露于10000勒克斯富含蓝光的发光二极管光下9小时后,显示出显著的细胞凋亡。总体而言,基因表达谱分析和定量聚合酶链反应(qPCR)表明,生长停滞和DNA损伤诱导蛋白45α(GADD45α)的表达明显上调。短暂敲低GADD45α可部分减轻光损伤诱导的ARPE - 19细胞凋亡,而GADD45α过表达则显著增加细胞凋亡。这些结果证明了GADD45α在光诱导的RPE细胞凋亡中的关键作用。定量逆转录PCR和蛋白质印迹分析显示,GADD45α的上调受p53的直接控制。此外,用AKT磷酸化抑制剂Ly294002处理,可进一步促进非光损伤和光损伤的ARPE - 19细胞中GADD45α基因的转录。该处理还加剧了光暴露后RPE细胞的凋亡,证实抑制Akt磷酸化可增加GADD45α的表达。总体而言,我们的研究结果表明,光照射通过上调由p53和磷脂酰肌醇3 -激酶 - AKT信号通路介导的GADD45α表达,诱导人类RPE细胞凋亡。这些结果为光损伤引发的人类视网膜疾病提供了新的见解,并为疾病的预防和治疗开辟了新途径。