Globular adiponectin protects human umbilical vein endothelial cells against apoptosis through adiponectin receptor 1/adenosine monophosphate-activated protein kinase pathway

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	Globular adiponectin protects human umbilical vein endothelial cells against apoptosis through adiponectin receptor 1/adenosine monophosphate-activated protein kinase pathway
其他题名	Globular adiponectin protects human umbilical vein endothelial cells against apoptosis through adiponectin receptor 1/adenosine monophosphate-activated protein kinase pathway
	Zhao Hongyu 1; Zhao Min 1; Yi Tongning 2; Zhang Jin 1
	2011
发表期刊	CHINESE MEDICAL JOURNAL
ISSN	0366-6999
卷号	124 期号:16 页码:2540-2547
摘要	Background Endothelial dysfunction is a key event in the onset and progression of atherosclerosis in diabetic patients. Apoptosis may lead to endothelial dysfunction and contribute to vascular complications. However, no study has addressed apoptosis in human umbilical vein endothelial cells (HUVECs) induced by an intermittent high-glucose media and its association with adiponectin receptor 1 (adipoR1), adipoR2, or adenosine monophosphate (AMP)-activated protein kinase (AMPK).
其他摘要	Background Endothelial dysfunction is a key event in the onset and progression of atherosclerosis in diabetic patients. Apoptosis may lead to endothelial dysfunction and contribute to vascular complications. However, no study has addressed apoptosis in human umbilical vein endothelial cells (HUVECs) induced by an intermittent high-glucose media and its association with adiponectin receptor 1 (adipoR1), adipoR2, or adenosine monophosphate (AMP)-activated protein kinase (AMPK). Methods HUVECs were cultured in continuous normal glucose (5.5 mmol/L), continuous high glucose (25 mmol/L), alternating normal and high glucose and mannitol. In the alternating normal and high-glucose media, HUVECs were treated under different conditions. First, cells were transfected with the adipoRl-specific small-interfering RNA (siRNA) and then stimulated with globular adiponectin (gAD). Second, cells were cultured in both gAD and the AMPK activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR). Third, cells were cultured in the AMPK inhibitor adenine-9-β-D-arabino-furanoside (araA), gAD, and in AICAR. Results HUVEC apoptosis increased more significantly in an intermittent high-glucose medium than in a constant high-glucose medium. HUVEC apoptosis induced by an intermittent high-glucose medium was inhibited when the cells were pretreated with 3 μg/ml gAD, which rapidly activated AMPK and adipoR1 in HUVECs. However, adipoR2 was not activated. Conclusions We found that adipoR1, not adipoR2, is involved in mediating intermittent high-concentration glucoseevoked apoptosis in endothelial cells. gAD activated AMPK through adipoR1, leads to the partial inhibition of HUVEC apoptosis. A fluctuating glucose medium is more harmful than a constant high-glucose medium to endothelial cells.
关键词	CORONARY-ARTERY-DISEASE FATTY-ACID OXIDATION GLUCOSE ENHANCES APOPTOSIS LOW-DENSITY-LIPOPROTEIN DIABETIC MICE UP-REGULATION MUSCLE-CELLS EXPRESSION MACROPHAGES SUPPRESSION globular adiponectin adiponectin receptor 1 AMP-activated protein kinase apoptosis intermittent glucose
收录类别	CSCD
语种	英语
CSCD记录号	CSCD:4325356
引用统计	被引频次：2[CSCD] [CSCD记录]
文献类型	期刊论文
条目标识符	http://ir.imr.ac.cn/handle/321006/152150
专题	中国科学院金属研究所
作者单位	1.中国科学院金属研究所 2.辽宁大学
推荐引用方式 GB/T 7714	Zhao Hongyu,Zhao Min,Yi Tongning,et al. Globular adiponectin protects human umbilical vein endothelial cells against apoptosis through adiponectin receptor 1/adenosine monophosphate-activated protein kinase pathway[J]. CHINESE MEDICAL JOURNAL,2011,124(16):2540-2547.
APA	Zhao Hongyu,Zhao Min,Yi Tongning,&Zhang Jin.(2011).Globular adiponectin protects human umbilical vein endothelial cells against apoptosis through adiponectin receptor 1/adenosine monophosphate-activated protein kinase pathway.CHINESE MEDICAL JOURNAL,124(16),2540-2547.
MLA	Zhao Hongyu,et al."Globular adiponectin protects human umbilical vein endothelial cells against apoptosis through adiponectin receptor 1/adenosine monophosphate-activated protein kinase pathway".CHINESE MEDICAL JOURNAL 124.16(2011):2540-2547.