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C1q/TNF-Related Protein-9 Ameliorates Ox-LDL-Induced Endothelial Dysfunction via PGC-1α/AMPK-Mediated Antioxidant Enzyme Induction.
Sun, Haijian; Zhu, Xuexue; Zhou, Yuetao; Cai, Weiwei; Qiu, Liying.
Afiliación
  • Sun H; Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. haijsunjiangnan@jiangnan.edu.cn.
  • Zhu X; Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. xxzjn@jiangnan.edu.cn.
  • Zhou Y; Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. yuetao.zhou@jiangnan.edu.cn.
  • Cai W; Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. vivi_cha@jiangnan.edu.cn.
  • Qiu L; Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. qiulydoc@jiangnan.edu.cn.
Int J Mol Sci ; 18(6)2017 May 26.
Article en En | MEDLINE | ID: mdl-28587104
Oxidized low-density lipoprotein (ox-LDL) accumulation is one of the critical determinants in endothelial dysfunction in many cardiovascular diseases such as atherosclerosis. C1q/TNF-related protein 9 (CTRP9) is identified to be an adipocytokine with cardioprotective properties. However, the potential roles of CTRP9 in endothelial function remain largely elusive. In the present study, the effects of CTRP9 on the proliferation, apoptosis, migration, angiogenesis, nitric oxide (NO) production and oxidative stress in human umbilical vein endothelial cells (HUVECs) exposed to ox-LDL were investigated. We observed that treatment with ox-LDL inhibited the proliferation, migration, angiogenesis and the generation of NO, while stimulated the apoptosis and reactive oxygen species (ROS) production in HUVECs. Incubation of HUVECs with CTRP9 rescued ox-LDL-induced endothelial injury. CTRP9 treatment reversed ox-LDL-evoked decreases in antioxidant enzymes including heme oxygenase-1 (HO-1), nicotinamide adenine dinucleotide phosphate (NAD(P)H) dehydrogenase quinone 1, and glutamate-cysteine ligase (GCL), as well as endothelial nitric oxide synthase (eNOS). Furthermore, CTRP9 induced activation of peroxisome proliferator-activated receptor γ co-activator 1α (PGC1-α) and phosphorylation of adenosine monophosphate-activated protein kinase (AMPK). Of interest, AMPK inhibition or PGC1-α silencing abolished CTRP9-mediated antioxidant enzymes levels, eNOS expressions, and endothelial protective effects. Collectively, we provided the first evidence that CTRP9 attenuated ox-LDL-induced endothelial injury by antioxidant enzyme inductions dependent on PGC-1α/AMPK activation.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Glicoproteínas / Endotelio / Adiponectina / Proteínas Quinasas Activadas por AMP / Coactivador 1-alfa del Receptor Activado por Proliferadores de Peroxisomas gamma / Lipoproteínas LDL / Antioxidantes Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2017 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Glicoproteínas / Endotelio / Adiponectina / Proteínas Quinasas Activadas por AMP / Coactivador 1-alfa del Receptor Activado por Proliferadores de Peroxisomas gamma / Lipoproteínas LDL / Antioxidantes Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2017 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza