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Down-regulated miR-187 promotes oxidative stress-induced retinal cell apoptosis through P2X7 receptor
- Zhang, Qiu-Li, Wang, Wei, Alatantuya,, Dongmei,, Lu, Zhan-Jun, Li, Lan-Lan, Zhang, Tian-Zi
- International journal of biological macromolecules 2018 v.120 pp. 801-810
- 3' untranslated regions, animal models, apoptosis, hypertension, malondialdehyde, microRNA, oxidative stress, reactive oxygen species, retina, retinal diseases, tissues
- Several microRNAs (miRNAs) expressed in the retina were confirmed to involve in retinal cell apoptosis, which was closely linked with the development of retinal diseases. Our previous studies have confirmed a vital role of miR-187 in retinal cells apoptosis. The aim of this study was to further elucidate the precise role of miR-187 and its probable mechanisms in RGC-5 cells apoptosis. The cellular oxidative stress status was assessed by reactive oxygen species (ROS) production and malondialdehyde (MDA) level. Our results showed that the elevated pressure, glutamate and H2O2-induced oxidative stress in RGC-5 cells was accompanied by a decrease in miR-187 expression and an increase in P2X7R expression. However, overexpression of miR-187 reversed this activation of oxidative stress in RGC-5 cells. Moreover, we also revealed that miR-187 inhibited the oxidative stress-induced apoptosis of RGC-5 cells through negative regulating P2X7R, probably through interacting with the 3′UTR of P2X7R. Finally, we confirmed that the forced miR-187 expression alleviated oxidative stress injury in retina tissues of rat models with chronic ocular hypertension. Our data demonstrated that miR-187/P2X7R signaling was involved in retinal cell apoptosis, at least in part, through activating oxidative stress.