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Updated: Aug 14, 2025
Transpupillary Two-Photon In Vivo Imaging of the Mouse Retina
Published on: February 13, 2021
Long noncoding RNA uc007nnj.1 mediates neuronal death induced by retinal ischemia/reperfusion in mice via the
Yuqing Feng1,2, Jinfang Lu1,2, Xujun Peng1,2
1Department of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.
Background:
Retinal 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.
Methods:
Hank'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.
Results:
In 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.
Discussion:
Mechanistically, 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.
Conclusions:
Finally, 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.
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