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Inhibition of endoplasmic reticulum stress improves coronary artery function in type 2 diabetic mice.

 Soo-Kyoung Choi  ;  Mihwa Lim  ;  Soo-In Yeon  ;  Young-Ho Lee 
 EXPERIMENTAL PHYSIOLOGY, Vol.101(6) : 768-777, 2016 
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Animals ; Blood Glucose/physiology ; Body Weight/physiology ; Coronary Vessels/physiopathology* ; Diabetes Mellitus, Experimental/physiopathology* ; Diabetes Mellitus, Type 2/physiopathology* ; Endoplasmic Reticulum/physiology* ; Endoplasmic Reticulum Stress/physiology* ; Endothelium, Vascular/physiopathology ; Male ; Mice ; Phosphorylation/physiology
NEW FINDINGS: What is the central question of this study? Endoplasmic reticulum (ER) stress has been reported to be involved in type 2 diabetes; however, the role of exacerbated ER stress in vascular dysfunction in type 2 diabetes remains unknown. What is the main finding and its importance? The main findings of this study are that ER stress is increased in the coronary arteries in type 2 diabetes, and inhibition of ER stress using taurine-conjugated ursodeoxycholic acid improves vascular function, which is associated with normalization of the myogenic response and endothelium-dependent relaxation. Vascular dysfunction is a major complication in type 2 diabetes. Although endoplasmic reticulum (ER) stress has been suggested to be a contributory factor in cardiovascular diseases, the relationship between ER stress and vascular dysfunction in type 2 diabetes remains unclear. Thus, in the present study, we examined whether ER stress contributes to coronary artery dysfunction and whether inhibition of ER stress ameliorates vascular function in type 2 diabetes. Type 2 diabetic mice and their control counterparts were treated with an ER stress inhibitor (taurine-conjugated ursodeoxycholic acid, 150 mg kg(-1) day(-1) , by i.p. injection) for 2 weeks or not treated. The myogenic response and endothelium-dependent relaxation were measured in pressurized coronary arteries. In type 2 diabetic mice, blood glucose and body weight were elevated compared with control mice. The myogenic response was potentiated and endothelium-dependent relaxation impaired in coronary arteries from the type 2 diabetic mice. Interestingly, treatment with the ER stress inhibitor normalized the myogenic responses and endothelium-dependent relaxation. These data were associated with an increase in ER stress marker expression or phosphorylation (IRE1-XBP-1 and PERK-eIF2α) in type 2 diabetic mice, which were reduced by treatment with the ER stress inhibitor. Inhibition of ER stress normalizes the myogenic response and improves vascular function in type 2 diabetes. Therefore, ER stress could be a potential target for cardiovascular diseases in diabetes mellitus.
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1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Lee, Young Ho(이영호) ORCID logo https://orcid.org/0000-0002-5749-1045
Lim, Mi Hwa(임미화)
Choi, Soo Kyoung(최수경) ORCID logo https://orcid.org/0000-0002-7115-6358
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