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   <subfield code="a">Clopidogrel reduces apoptosis and promotes proliferation of human vascular endothelial cells induced by palmitic acid via suppression of the long non-coding RNA HIF1A-AS1 in vitro</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Jing Wang, Lingqiang Chen, Hongfei Li, Jin Yang, Zhiqiang Gong, Bing Wang, Xueling Zhao]</subfield>
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   <subfield code="a">Cardiovascular disease (CVD) is recognized as a major and increasing health problem affected older subjects in China, and clopidogrel has been widely used for treatment of CVD patients such as atherosclerosis, myocardial infarction, and myocardial ischaemia-reperfusion damage. However, the molecular mechanisms of clopidogrel for treatment of CVD are only partially understood. This study investigated the effects of clopidogrel on palmitic acid-induced damage of human vascular endothelial cells (HUVECs), and the molecular mechanisms of LncRNA HIF1A-AS1 in regulating the proliferation and apoptosis of HUVECs in vitro. We firstly established a damage model of HUVECs through palmitic acid (PA) treatment. And the effect of clopidogrel reducing PA-induced apoptosis of HUVECs was observed by the flow cytometric measurement. To further understand the molecular mechanism of clopidogrel rescues PA-induced apoptosis, we used human LncRNA PCR array to compare the LncRNA expression profile difference between clopidogrel-treated cells and control cells. The expression of LncRNA HIF 1 alpha-antisense RNA 1 (HIF1A-AS1) was significantly altered in clopidogrel-treated cells. We further proved that suppression of HIF1A-AS1 by siRNA reduce PA-induced apoptosis and promote proliferation of HUVECs. Furthermore, we also demonstrated inhibition apoptosis effect by HIF1A-AS1 is related to mitochondrial apoptosis pathway. Hence, our results suggest that clopidogrel rescues apoptosis and promotes proliferation of PA-induced damage model of HUVECs through inhibiting the mediator LncRNA HIF1A-AS1. These findings indicate that LncRNA HIF1A-AS1 may play an important role in the pathogenesis of CVD, and provide a novel molecular mechanism of clopidogrel for treatment of CVD.</subfield>
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   <subfield code="a">Springer Science+Business Media New York, 2015</subfield>
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   <subfield code="a">Human vascular endothelial cells</subfield>
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   <subfield code="a">Palmitic acid</subfield>
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   <subfield code="a">Bcl 2-caspase 9-caspase 3 pathway</subfield>
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   <subfield code="a">Wang</subfield>
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   <subfield code="u">Department of Rheumatology, The First People's Hospital of Yunnan Province, Kunming, Yunnan, China</subfield>
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   <subfield code="a">Chen</subfield>
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   <subfield code="u">Department of Orthopaedics, The First Affiliated Hospital of Kunming Medical University, No. 295, Xichang Road, 650032, Kunming, Yunnan, China</subfield>
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   <subfield code="a">Li</subfield>
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   <subfield code="u">Department of Orthopaedics, The First Affiliated Hospital of Kunming Medical University, No. 295, Xichang Road, 650032, Kunming, Yunnan, China</subfield>
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   <subfield code="t">Molecular and Cellular Biochemistry</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
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