Horm Metab Res 2015; 47(02): 107-113
DOI: 10.1055/s-0034-1385871
Endocrine Research
© Georg Thieme Verlag KG Stuttgart · New York

Life and Death of Human Vascular Endothelial Cells by Stimulation with Free Fatty Acids Through Death Receptors

X.-R. Zhan
1   Department of Endocrinology, Chinese PLA General Hospital, Beijing, P. R. China
2   Department of Endocrinology, First affiliated Hospital, Harbin Medical University, Harbin, P. R. China
,
Y.-M. Mu
1   Department of Endocrinology, Chinese PLA General Hospital, Beijing, P. R. China
,
C.-Y Pan
1   Department of Endocrinology, Chinese PLA General Hospital, Beijing, P. R. China
,
Y.-J. Xiao
1   Department of Endocrinology, Chinese PLA General Hospital, Beijing, P. R. China
,
Z.-Q. Lu
1   Department of Endocrinology, Chinese PLA General Hospital, Beijing, P. R. China
,
F.-H. Liu
1   Department of Endocrinology, Chinese PLA General Hospital, Beijing, P. R. China
,
X.-Y. Li
2   Department of Endocrinology, First affiliated Hospital, Harbin Medical University, Harbin, P. R. China
,
J.-J. Yu
2   Department of Endocrinology, First affiliated Hospital, Harbin Medical University, Harbin, P. R. China
› Author Affiliations
Further Information

Publication History

received after second revision09 July 2014

accepted 09 July 2014

Publication Date:
17 September 2014 (online)

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Abstract

Diabetic individuals may have elevated levels of serum free fatty acids and may exhibit injury to the vascular endothelial cells. This study was undertaken to determine the relationship between various free fatty acids (FFAs) and vascular endothelial cell injury and the molecular mechanisms linking FFA-induced vascular endothelial cells injury or protection. We observed the survival of HUVECs exposed to different FFAs, and our results revealed that the effects of various FFAs on the cell survival of HUVECs were significantly different. Palmitic acid (PA) markedly decreased the HUVEC survival rate in a time- and dose-dependent manner, but arachidonic acid (AA) significantly increased the cell survival rate and could partially prevent cellular apoptosis induced by PA. Interestingly, PA and AA could activate the same target receptor, TNF-R1. PA induced the apoptosis of HUVECs by initiating the death pathway (TNF-R1/TRADD/caspases 8 pathway), whereas AA enhanced cell survival to protect vascular endothelial cells by activating the survival pathway (TNF-R1/RIP/NF-κB 50/NF-κB 65).

* These authors contributed equally to this study.