RNCR3 knockdown inhibits diabetes mellitus-induced retinal reactive gliosis.
Retinal reactive gliosis is an important pathological feature of diabetic retinopathy. Identifying the underlying mechanisms causing reactive gliosis will be important for developing new therapeutic strategies for treating diabetic retinopathy. Herein, we show that long noncoding RNA-RNCR3 knockdown significantly inhibits retinal reactive gliosis. RNCR3 knockdown leads to a marked reduction in the release of several cytokines. RNCR3 knockdown alleviates diabetes mellitus-induced retinal neurodegeneration, as shown by less apoptotic retinal cells and ameliorative visual function. RNCR3 knockdown could also decrease Müller glial cell viability and proliferation, and reduce the expression of glial reactivity-related genes including GFAP and vimentin in vitro. Collectively, this study shows that RNCR3 knockdown may be a promising strategy for the prevention of diabetes mellitus-induced retinal neurodegeneration.
Research Center, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China; Shanghai Key Laboratory of Visual Impairment and Restoration, Shanghai, China; The Fourth School of Clinical Medicine, Nanjing Medical University, Nanjing, China.
Chang
C
Liu
Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China.
Chao-Peng
CP
Li
Department of Ophthalmology, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Jia-Jian
JJ
Wang
Research Center, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China; Shanghai Key Laboratory of Visual Impairment and Restoration, Shanghai, China; The Fourth School of Clinical Medicine, Nanjing Medical University, Nanjing, China.
Kun
K
Shan
Research Center, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China; Shanghai Key Laboratory of Visual Impairment and Restoration, Shanghai, China.
Xin
X
Liu
Research Center, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China; Shanghai Key Laboratory of Visual Impairment and Restoration, Shanghai, China. Electronic address: biao.yan@fdeent.org.
Biao
B
Yan
D000818:Animals; D017209:Apoptosis / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics; D002470:Cell Survival / Q000235:genetics; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000235:genetics / Q000378:metabolism*; D004596:Electroretinography; D005455:Fluorescent Antibody Technique; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism; D005911:Gliosis / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000235:genetics*; D009457:Neuroglia / Q000378:metabolism; D034622:RNA Interference; D062085:RNA, Long Noncoding / Q000235:genetics*; D012160:Retina / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014746:Vimentin / Q000235:genetics / Q000378:metabolism
D016207:Cytokines; D005904:Glial Fibrillary Acidic Protein; D035683:MicroRNAs; C540079:Mirn124 microRNA, mouse; D062085:RNA, Long Noncoding; D014746:Vimentin
Diabetic retinopathy; Long noncoding RNA; Retinal reactive gliosis