Angiotensin II type 1 receptor autoantibodies induces INS-1 islet β-cell apoptosis by upregulation of autophagy
10.3969/j.issn.1000-4718.2018.03.016
- VernacularTitle:血管紧张素II1型受体自身抗体通过上调自噬诱导INS-1胰岛β细胞凋亡
- Author:
Dan LI
1
;
Jin WANG
;
Jin-Ling HE
;
Yan-Jin FENG
;
Zhu-Jie CAO
;
Xiang-Ying JIAO
Author Information
1. 山西医科大学生理学教研室
- Keywords:
Angiotensin Ⅱtype 1 receptor autoantibody;
INS-1 cells;
Apoptosis;
Autophagy
- From:
Chinese Journal of Pathophysiology
2018;34(3):474-480
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore whether the angiotensin II type 1 receptor autoantibodies(AT1-AA)induces islet β-cell apoptosis and whether autophagy is involved in the process.METHODS:The INS-1 cells treated with AT1-AA at 10-6mol/L for 24 h,and then the apoptosis was analyzed by flow cytometry,Western blot and Hoechst 33258 staining.In addition,the expression of autophagy-related proteins such as LC3 and beclin 1 were determined by Western blot.The effects of AT1-AA on the apoptosis,autophagy and viability of INS-1 cells with or without 3-methyladenine(3-MA;a com-mon autophagy inhibitor)or telmisartan(an angiotensin Ⅱ type 1 receptor blocker)pretreatment, were detected by flow cytometry,Western blot and CCK-8 assay.RESULTS: Treatment with AT1-AA at 10 -6mol/L for 24 h significantly re-duced the cell viability(P<0.05).Compared with the negative IgG control group,the apoptotic cells increased after incu-bation with AT1-AA for 12 h,24 h and 36 h,respectively(P<0.05).Moreover,the protein levels of LC3 and beclin 1 also increased gradually with the prolongation of treatment time,and the elevation of apoptosis and autophagy were blocked by telmisartan.After pretreatment with 3-MA, the apoptotic rate of the cells was obviously decreased compared with the cells treated with AT1-AA alone.CONCLUSION: AT1-AA induces the apoptosis of INS-1 islet βcells by upregulating autophagy via the angiotensin Ⅱtype 1 receptor pathway.
