Sun Ting-Ting, Li Xiu-Miao, Zhu Jun-Ya, Yao Wen, Yang Tian-Jing, Meng Xiang-Rui, Yao Jin, Jiang Qin
The Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China.
The Fourth School of Clinical Medicine, Nanjing Medical University, Nanjing, China.
Heliyon. 2022 Oct 10;8(10):e10994. doi: 10.1016/j.heliyon.2022.e10994. eCollection 2022 Oct.
Ischemia/reperfusion (I/R) injury is a common pathological mechanism involved in many ocular diseases. I/R is characterized by microvascular dysfunction and neurodegeneration. However, the mechanisms of neurodegeneration induced by I/R remain largely unknown. This study showed that the expression of long non-coding RNA-CRNDE was significantly upregulated after retinal ischemia-reperfusion (RIR). LncRNA-CRNDE knockdown alleviated retinal neurodegeneration induced by RIR injury, as shown by decreased reactive gliosis and reduced retinal cells loss. Furthermore, lncRNA-CRNDE knockdown directly regulated Müller cell function and indirectly affected RGC function . In addition, lncRNA-CRNDE knockdown led to a significant reduction in the release of several cytokines after RIR. This study suggests that lncRNA-CRNDE is a promising therapeutic target for RIR.
缺血/再灌注(I/R)损伤是许多眼部疾病中常见的病理机制。I/R的特征是微血管功能障碍和神经变性。然而,I/R诱导神经变性的机制在很大程度上仍然未知。本研究表明,视网膜缺血-再灌注(RIR)后长链非编码RNA-CRNDE的表达显著上调。如反应性胶质细胞增生减少和视网膜细胞损失减少所示,lncRNA-CRNDE敲低减轻了RIR损伤诱导的视网膜神经变性。此外,lncRNA-CRNDE敲低直接调节穆勒细胞功能并间接影响视网膜神经节细胞功能。此外,lncRNA-CRNDE敲低导致RIR后几种细胞因子的释放显著减少。本研究表明,lncRNA-CRNDE是RIR的一个有前景的治疗靶点。