Please use this identifier to cite or link to this item: https://doi.org/10.3390/ijms18061097
Title: C1q/TNF-related protein-9 ameliorates Ox-LDL-induced endothelial dysfunction via PGC-1²/AMPK-mediated antioxidant enzyme induction
Authors: Sun, H 
Zhu, X
Zhou, Y
Cai, W
Qiu, L
Keywords: complement component C1q
CXCL11 chemokine
endothelial nitric oxide synthase
glutamate cysteine ligase
heme oxygenase 1
nicotinamide adenine dinucleotide phosphate
nitric oxide
oxidized low density lipoprotein
peroxisome proliferator activated receptor gamma coactivator 1alpha
reactive oxygen metabolite
small interfering RNA
tumor necrosis factor
adiponectin
antioxidant
C1QTNF9B protein, human
endothelial nitric oxide synthase
glycoprotein
hydroxymethylglutaryl coenzyme A reductase kinase
low density lipoprotein
peroxisome proliferator activated receptor gamma coactivator 1alpha
PPARGC1A protein, human
reactive oxygen metabolite
agar gel electrophoresis
apoptosis
Article
cell culture
cell cycle assay
cell migration assay
cell proliferation assay
controlled study
cytotoxicity
endothelial dysfunction
endothelium injury
genetic transfection
human
human cell
immunofluorescence test
oxidative stress
protein expression
TUNEL assay
umbilical vein endothelial cell
Western blotting
cell cycle
cell motion
cell proliferation
drug effects
endothelium
metabolism
oxidation reduction reaction
oxidative stress
pathophysiology
Adiponectin
AMP-Activated Protein Kinases
Antioxidants
Apoptosis
Cell Cycle
Cell Movement
Cell Proliferation
Endothelium
Glycoproteins
Human Umbilical Vein Endothelial Cells
Humans
Lipoproteins, LDL
Nitric Oxide
Nitric Oxide Synthase Type III
Oxidation-Reduction
Oxidative Stress
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
Reactive Oxygen Species
Issue Date: 2017
Publisher: MDPI
Citation: Sun, H, Zhu, X, Zhou, Y, Cai, W, Qiu, L (2017). C1q/TNF-related protein-9 ameliorates Ox-LDL-induced endothelial dysfunction via PGC-1²/AMPK-mediated antioxidant enzyme induction. International Journal of Molecular Sciences 18 (6) : 1097. ScholarBank@NUS Repository. https://doi.org/10.3390/ijms18061097
Rights: Attribution 4.0 International
Abstract: 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 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. © 2017 by the authors. Licensee MDPI, Basel, Switzerland.
Source Title: International Journal of Molecular Sciences
URI: https://scholarbank.nus.edu.sg/handle/10635/183522
ISSN: 1661-6596
DOI: 10.3390/ijms18061097
Rights: Attribution 4.0 International
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