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Stimulation of autophagy improves vascular function in the mesenteric arteries of type 2 diabetic mice

Authors
 Soo‐Kyoung Choi  ;  Youngin Kwon  ;  Seonhee Byeon  ;  Young‐Ho Lee 
Citation
 EXPERIMENTAL PHYSIOLOGY, Vol.105(1) : 192-200, 2020 
Journal Title
 EXPERIMENTAL PHYSIOLOGY 
ISSN
 0958-0670 
Issue Date
2020
Keywords
autophagy ; endothelium-dependent relaxation ; mesenteric artery ; myogenic response ; type 2 diabetes ; vascular dysfunction
Abstract
NEW FINDINGS: What is the central question of this study? What is the role of autophagy in vascular dysfunction in type 2 diabetes? What is the main finding and its importance? Autophagy is decreased in the mesenteric arteries of type 2 diabetic mice, and stimulation of autophagy using rapamycin and trehalose improves vascular function, which is associated with normalization of myogenic response and endothelium-dependent relaxation. ABSTRACT: Vascular dysfunction is a major complication in type 2 diabetes (T2D). It has been suggested that dysregulation of autophagy is associated with various cardiovascular diseases. However, the relationship between autophagy and vascular dysfunction in T2D remains unclear. Thus, we examined whether reduced autophagy is involved in vascular dysfunction and whether stimulation of autophagy could improve vascular function in diabetes. Ten- to twelve-week-old male type 2 diabetic (db- /db- ) mice and their control (db- /db+ ) mice were treated with rapamycin or trehalose. Mesenteric arteries (MAs) were mounted for arteriography and their diameter was measured. Western blot analysis and immunofluorescence staining were assessed. Myogenic response (MR) was significantly increased, whereas endothelium-dependent relaxation (EDR) was significantly attenuated in the MAs of diabetic mice. These results were associated with increased expression of LC3II, p62 and beclin-1 in diabetic mice. Treatment with autophagy stimulators significantly reduced the potentiation of MR and improved EDR in the diabetic mice. Furthermore, autophagy stimulation normalized expression of LC3II, p62 and beclin-1 in the diabetic mice. In addition, phosphorylation level of endothelial nitric oxide synthase was decreased in diabetic mice and was restored by rapamycin and trehalose. T2D impairs vascular function by dysregulated autophagy. Therefore, autophagy could be a potential target for overcoming diabetic microvascular complications.
Full Text
https://physoc.onlinelibrary.wiley.com/doi/full/10.1113/EP087737
DOI
10.1113/EP087737
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Byeon, Seon Hee(변선희) ORCID logo https://orcid.org/0000-0001-9256-5209
Lee, Young Ho(이영호) ORCID logo https://orcid.org/0000-0002-5749-1045
Choi, Soo Kyoung(최수경) ORCID logo https://orcid.org/0000-0002-7115-6358
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/174886
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