下调和上调
细胞生物学
自噬
感光细胞
外体
视网膜变性
安普克
微泡
医学
视网膜
细胞凋亡
生物
小RNA
蛋白激酶A
生物化学
神经科学
激酶
基因
作者
Xiang Ren,Jinjuan Lv,Nina Wang,Junli Liu,Chuanzhou Gao,Xiaoli Wu,Yang Yu,Qiufeng Teng,Wenkang Dong,Hui Kong,Li Kong
标识
DOI:10.1016/j.diabres.2022.109788
摘要
Abstract
Aims
Autophagy and exosome secretion in photoreceptor and RPE cells play an important role during diabetic retinopathy (DR). Thioredoxin (Trx) upregulation delays diabetes-induced photoreceptor cell degeneration, which the effect of autophagy and exosome secretion on it is unclear. Therefore, we investigated the effect of them on Trx upregulation to delay diabetes-induced photoreceptor cell degeneration and to identify the potential therapy for DR in the future. Methods
Trx-transgenic mice and 661w cell were as models. Retinal function and morphology were evaluated by electroretinography and H&E staining. TUNEL staining was used to evaluate apoptosis. The protein expression was detected by Western blotting. TEM and mRFP-GFP-LC3 method were used to analyze autophagy. Results
In vitro and in vivo, Trx upregulation can delay diabetes-induced photoreceptor cell degeneration. Moreover, the expression of LC3 and p62 was decreasing and the expression of Alix and CD63 was increasing after Trx overexpression. However, it was inhibited after AMPK inhibitor treatment. Additionally, secreted exosomes from photoreceptor were phagocytosed by RPE cells to regulate its physiological function. Conclusions
Trx upregulation can delay diabetes-induced photoreceptor cell degeneration via AMPK-mediated autophagy and exosome secretion. Secreted exosomes from photoreceptor cells could be phagocytosed and degraded by RPE cells in DR.
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