机构：[1]Affiliated Eye Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Jiangxi Research Institute of Ophthalmology and Visual Science, Jiangxi Provincial Key Laboratory for Ophthalmology, Jiangxi Clinical Research Center for Ophthalmic Disease, Nanchang, China.[2]Department of Orthopaedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.[3]Medical School of Chinese PLA, Beijing, China.[4]Department of Ophthalmology, The Second Xiangya Hospital of Central South University, Changsha, China.[5]State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.[6]Institute of Translational Medicine, Nanchang University, Nanchang, China.
The purpose of this study was to investigate the protective effect of CD38 deletion on retinal ganglion cells (RGCs) in a mouse retinal ischemia/reperfusion (I/R) model and an optic nerve crush (ONC) model, and to elucidate the underlying molecular mechanisms.Retinal I/R and ONC models were constructed in mice. PCR was used to identify the deletion of CD38 gene in mice, hematoxylin and eosin (H&E) staining was used to evaluate the changes in retinal morphology, and electroretinogram (ERG) was used to evaluate the changes in retinal function. The survival of RGCs and activation of retinal macroglia were evaluated by immunofluorescence staining. The expression of Sirt1, CD38, Ac-p65, Ac-p53, TNF-α, IL-1β, and Caspase3 proteins in the retina was further evaluated by protein imprinting.In retinal I/R and ONC models, CD38 deficiency reduced the loss of RGCs and activation of macroglia and protected the retinal function. CD38 deficiency increased the concentration of NAD+, reduced the degree of acetylation of NF-κB p65 and p53, and reduced expression of the downstream inflammatory cytokines TNFα, IL-1β, and apoptotic protein Caspase3 in the retina in the ONC model. Intraperitoneal injection of the Sirt1 inhibitor EX-527 partially counteracted the effects of CD38 deficiency, suggesting that CD38 deficiency acts at least in part through the NAD+/Sirt1 pathway.CD38 plays an important role in the pathogenesis of retinal I/R and ONC injury. CD38 deletion protects RGCs by attenuating inflammatory responses and apoptosis through the NAD+/Sirt1 pathway.
基金：
Supported by the National Natural Science Foundation of China
(Nos. 82260203) and the Talent Cultivation Program Fund of
Affiliated Eye Hospital of Nanchang University (Nos. 2022X01).
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2023]版：
大类|2 区医学
小类|2 区眼科学
最新[2023]版：
大类|2 区医学
小类|2 区眼科学
第一作者：
第一作者机构：[1]Affiliated Eye Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Jiangxi Research Institute of Ophthalmology and Visual Science, Jiangxi Provincial Key Laboratory for Ophthalmology, Jiangxi Clinical Research Center for Ophthalmic Disease, Nanchang, China.
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Pang Yulian,Hu Haijian,Xu Ke,et al.CD38 Deficiency Protects Mouse Retinal Ganglion Cells Through Activating the NAD+/Sirt1 Pathway in Ischemia-Reperfusion and Optic Nerve Crush Models[J].Investigative Ophthalmology & Visual Science.2024,65(5):36.doi:10.1167/iovs.65.5.36.
APA：
Pang Yulian,Hu Haijian,Xu Ke,Cao Ting,Wang Zhiruo...&Zhang Xu.(2024).CD38 Deficiency Protects Mouse Retinal Ganglion Cells Through Activating the NAD+/Sirt1 Pathway in Ischemia-Reperfusion and Optic Nerve Crush Models.Investigative Ophthalmology & Visual Science,65,(5)
MLA：
Pang Yulian,et al."CD38 Deficiency Protects Mouse Retinal Ganglion Cells Through Activating the NAD+/Sirt1 Pathway in Ischemia-Reperfusion and Optic Nerve Crush Models".Investigative Ophthalmology & Visual Science 65..5(2024):36
