Activation of paraptosis and autophagy in rat retina following acute retinal ischemia-reperfusion injury
10.13389/j.cnki.rao.2018.0117
- VernacularTitle:急性视网膜缺血再灌注损伤后大鼠视网膜副凋亡和自噬的发生
- Author:
Ting WEI
1
;
Shan GAO
;
Qiao-Chu CHENG
;
Li-Jun CUI
;
Qian-Yan KANG
Author Information
1. 西安交通大学第一附属医院眼科
- Keywords:
paraptosis;
autophagy;
retinal ischemia-reperfusion injury;
retinal ganglion cells
- From:
Recent Advances in Ophthalmology
2018;38(6):501-505
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate whether paraptosis and autophagy have an effect on acute retinal ischemia-reperfusion injury (RIRI) in an experimental rat model that recapitulates features of acute hypertensive glaucoma and to explore the possible underlying mechanisms.Methods A total of 30 adult male Sprague-Dawley rats were randomly divided into RIRI group and control group.The acute RIRI model was induced with normal saline in the right eye of rats from the RIRI group by anterior chamber perfusion,while the rats in the control group left untreated.On day 1,day 3,day 7,day 28 after RIRI model establishment,the changes in morphology of retinal ganglion cells (RGCs) were observed by transmission electron microscopy (TEM),and the expression of microtubule-associated protein 1 light chain 3 (LC3) was measured by immumofluorescence methods.Results When compared with the control group,the number of cytoplasmic vacuoles predominantly derived from the progressive swelling of mitochondria and/or endoplasmic reticulum (ER) in RGCs were increased in the RIRI group from day 1 to day 28 by TEM.And ultra-structural analyses showed the double-or multiple-membrane autophagosomes were markedly accumulated in the cytoplasm of RGCs following acute RIRI.The average number of autophagic vacuoles in the cytoplasm of RGCs was 0.79 per 50 μm2 in the control group,and the average number of autophagosomes reached to a maximum on day 7 after acute RIRI at 2.29 per 50 μm2,which was statistically significant compared with the control group (P ＜ 0.05).Compared to the control group,LC3 expression in the cytoplasm of RGCs was up-regulated on day 1 after acute RIRI,which sustained throughout the experimental period.The percentage of LC3 positive cells in the retinal ganglion cell layer was 15.90％ in the control group,and the data was 46.95％ and 52.30％ on day 1 and day 28 after RIRI,respectively,both which were statistically significant compared with the normal control group (both P ＜ 0.05).Conclusion Both paraptosis and autophagy participate in death of RGCs after acute RIRI.Programmed cell death in different cells,either coexistence of multiple-cell death form or a single-cell death form,participates in the pathogenesis of acute RIRI.
