Long noncoding RNA uc007nnj.1 mediates neuronal death induced by retinal ischemia/reperfusion in mice via the miR-155-5p/Tle4 axis

Molecular Medicine

Research Article

Xujun Peng¹  Jinfang Lu¹  Yanni Ge¹  Yuqing Feng¹  Huiling Li¹  Ran Zhang¹ 

[1] Department of Ophthalmology, The Second Xiangya Hospital, Central South University, 410011, Changsha, Hunan, China;Hunan Clinical Research Center of Ophthalmic Disease, 410011, Changsha, Hunan, China;

关键词: lncRNA uc007nnj.1;    I/R;    RGCs;    Apoptosis;    miR-155-5p;   

DOI  :  10.1186/s10020-022-00591-5

 received in 2022-03-10, accepted in 2022-12-13,  发布年份 2022

来源: Springer

【 摘 要 】

BackgroundRetinal ganglion cells (RGCs) apoptosis is a vital manifestation of retinal ischemia/reperfusion (I/R) injury, yet the underlying mechanisms are not well understood. The contribution of long noncoding RNAs (lncRNAs) to this cellular process is currently being explored. Based on a lncRNA chip assay, we aimed to investigate the role of lncRNA uc007nnj.1 in the pathological process of ischemia-induced RGCs apoptosis.MethodsHank’s balanced salt solution containing 10 µM antimycin A and 2 µM calcium ionophore for 2 h to construct an ischemic model in RGCs, and elevation of intraocular pressure to 120 mm Hg for 1 h was used to construct a mouse model of retinal I/R injury.ResultsIn this study, lncRNA uc007nnj.1 was highly upregulated in response to I/R injury in RGCs and mouse retinas. In addition, lncRNA uc007nnj.1 knockdown reduced retinal neuronal cell apoptosis in vitro and in vivo and significantly improved retinal function.DiscussionMechanistically, the results demonstrated that lncRNA uc007nnj.1 acts as ceRNA competitively binding miR-155-5p, thereby enhancing the expression levels of Tle4, thus aggravating ischemia-related apoptosis in RGCs.ConclusionsFinally, our study identifies the lncRNA uc007nnj.1/miR-155-5p/Tle4 axis as a potential target for the prevention of I/R-induced retinal neuronal death.

【 授权许可】

CC BY   
© The Author(s) 2023

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