C1q/TNF-Related Protein-9 Ameliorates Ox-LDL-Induced Endothelial Dysfunction via PGC-1α/AMPK-Mediated Antioxidant Enzyme Induction

Sun, Hai-Jian; Zhu, Xiaofang; Zhou, Yuetao; Cai, Weiwei; Qiu, Ling

doi:10.3390/ijms18061097

Cited by 40 publications

(25 citation statements)

References 63 publications

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“…Although the cytotoxic effects of ox-LDL on vascular endothelial cells have been well-established, the exact role of ox-LDL in migratory capacity is still confusing. Sun et al, demonstrated that ox-LDL inhibited the migration of HUVECs by performing Transwell assay, without excluding the proliferation-inhibitory impacts of ox-LDL on the number of the migrated cells [23]. However, the opposite effect of ox-LDL has been reported by Bao et al, in the same cell line [24].…”

Section: Discussionmentioning

confidence: 80%

Notoginsenoside R1 Protects HUVEC Against Oxidized Low Density Lipoprotein (Ox-LDL)-Induced Atherogenic Response via Down-Regulating miR-132

Fu¹,

Yin²,

Nie³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Radix notoginseng is a well-known traditional Chinese herbal medicine, has extensively pharmacological activities in cardiovascular system. Notoginsenoside R1 (NGR1) is one main active ingredient of Radix notoginseng. The purpose of this study was to evaluate the functional effects of NGR1 on atherosclerosis (AS). Methods: Human umbilical vascular endothelial cells (HUVECs) were subjected to oxidized low density lipoprotein (ox-LDL), before which cells were preconditioned with NGR1. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, Transwell assay, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were carried out to assess the impacts of ox-LDL and NGR1 on HUVECs. Besides, the expression of microRNA-132 (miR-132), and the regulatory role of miR-132 in Matrix Gla Protein (MGP) expression were measured by qRT-PCR and Western blot. Results: NGR1 pre-conditioning prevented ox-LDL-induced apoptosis, migration and overproduction of Monocyte Chemoattractant Protein 1 (MCP-1) and Intercellular Adhesion Molecule 1 (ICAM-1). miR-132 was up-regulated in response to ox-LDL while was down-regulated by NGR1 pre-conditioning. The protective actions of NGR1 in ox-LDL-treated HUVECs were enhanced by miR-132 inhibitor, while were attenuated by miR-132 mimic. Besides, the up-regulated miR-132 could further decrease the expression of MGP, which acted as an anti-migratory and anti-adhesive factor. Furthermore, ox-LDL-induced the activation of c-Jun N-terminal Kinase (JNK) and Nuclear Factor Kappa B (NF-κB) pathways were partially attenuated by NGR1, and were fully eliminated by NGR1 treatment together with MGP overexpression. Conclusion: NGR1 prevents ox-LDL-induced apoptosis, migration and adhesion-related molecule release in HUVECs possibly via down-regulating miR-132, and subsequent up-regulating MGP.

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Section: Discussionmentioning

confidence: 80%

Notoginsenoside R1 Protects HUVEC Against Oxidized Low Density Lipoprotein (Ox-LDL)-Induced Atherogenic Response via Down-Regulating miR-132

Fu¹,

Yin²,

Nie³

et al. 2018

Cell Physiol Biochem

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“…Moreover, oxidized low density lipoprotein (Ox‐LDL) and hyperglycemia are crucial risk factors of endothelial dysfunction, both of which have the capacity of inhibiting the production of NO, promoting EC apoptosis, producing reactive oxygen species (ROS) and reducing mitochondria production. CTRP9 could attenuate ox‐LDL‐induced endothelial injury through antioxidant enzymes dependent on peroxisome proliferator activated receptor γ coactivator ‐1α (PGC‐1α) /AMPK activation (Sun, Zhu, Zhou, Cai, & Qiu, ) and may induce mitochondrial biogenesis and protect high glucose induced endothelial oxidative damage via AdipoR1/SIRT1/PGC‐1α signaling pathway (Cheng et al, ).…”

Section: Introductionmentioning

confidence: 99%

C1q/TNF‐related protein 9: A novel therapeutic target in ischemic stroke?

Yang

Fan

Sawmiller

et al. 2018

J of Neuroscience Research

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| INTRODUC TI ONIschemic stroke and coronary atherosclerosis disease (CAD) are both kinds of atherosclerotic diseases with high morbidity and high mortality, which have already been on the spotlight in both clinic and research. Vascular lesion is the major feature in the pathogenesis of these two diseases. Initially, the endothelial cells (EC) are damaged by risk factors, followed with activated platelets, inflammatory reactions, and accelerated vessel wall remodeling. Consequently, atherosclerotic plaques forming, rupture and erosion, with different subtypes of surface thrombosis, vasospasm and distal vascular embolization, lead to ischemic lesions, including ischemic stroke and CAD. However, the molecular mechanism of vascular lesion is complicated, which requires further research for the full understanding of pathogenesis of atherosclerotic diseases.C1q/TNF-related protein 9 (CTRP9) is a newly discovered adipokine. By searching databases of Medline and Web of Science (WOS), we found only a few reports about this factor, most of which were published in the past two years. Meanwhile, they mainly expounded the role of CTRP9 in the blood vessels related pathogenesis of CAD, including regulating energy metabolism, modulating vasomotion, protecting EC, inhibiting platelet activation, inhibiting pathological vascular remodeling, stabilizing atherosclerotic plaques, and protecting heart. Here, we reviewed the genic features, proteinic features and physiologic functions of CTRP9, and proposed some possible associations between CTRP9 and ischemic stroke as well. AbstractIschemic stroke has become a serious public health problem, which is in need of advanced research on the prevention and treatment. As a newly discovered adipokine, C1q/TNF-related protein 9 (CTRP9) plays a vital role in the pathogenesis of coronary atherosclerosis disease (CAD), including regulating energy metabolism, modulating vasomotion, protecting endothelial cells, inhibiting platelet activation, inhibiting pathological vascular remodeling, stabilizing atherosclerotic plaques, and protecting heart. The present review raised a critical question of whether CTRP9 could also have the capacity of protecting the brain tissue and decreasing the severity of brain lesions in the ischemic stroke since CAD and ischemic stroke are both the major subtypes of atherosclerotic vascular diseases which share a large of common pathogenesis in the vascular lesion particularly. Therefore, we proposed that CTRP9 could be a feasible biomarker and potential therapeutic target in ischemic stroke on the basis of the reviewed research reports. K E Y W O R D Sadipokine, coronary atherosclerosis disease, CTRP9, ischemic stroke | 129 YANG et al.

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“…Nitric oxide is the main vasodilating factor produced by eNOS in vascular endothelium, and it plays a crucial role in the maintenance of vascular homoeostasis and prevention of atherothrombotic events [17]. Furthermore, the expressions of AT1R and eNOS are regulated by AMPK and PGC-1α [18][19][20].…”

Section: Aspirin Treatmentmentioning

confidence: 99%

Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPARδ-AMPK-PGC-1αPathway in Dyslipidemic Conditions

Han

Lee

Jang

et al. 2020

BioMed Research International

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This study is aimed at elucidating how aspirin could systemically and simultaneously normalize nonalcoholic fatty liver disease (NAFLD) and atherosclerosis through both in vitro and in vivo studies in hyperlipidemic conditions. We evaluated the effects and mechanism of aspirin on the levels of various biomarkers related to NAFLD, atherosclerosis, and oxidative phosphorylation in cells and animals of hyperlipidemic conditions. The protein levels of biomarkers (PPARδ, AMPK, and PGC-1α) involved in oxidative phosphorylation in both the vascular endothelial and liver cells were elevated by the aspirin in hyperlipidemic condition. Also in the stimulation pathway of oxidative phosphorylation by aspirin, PPARδ was a superior regulator than AMPK and PGC-1α in HepG2 cells. In the vascular endothelial cells, the phosphorylated endothelial nitric oxide synthase level was increased by the treatment. The protein levels of biomarkers related to lipid synthesis were decreased by the treatment in the liver cells. In rabbits administered with cholesterol diet, the levels of triglyceride, HDLcholesterol, and alanine amino transferase in serums were ameliorated by the aspirin treatment, the levels of ATP and TNFα were increased or decreased, respectively, by the aspirin in liver and aorta tissues, and mannose receptor and C-C chemokine receptor type 2 levels were increased or decreased by the aspirin in spleen, respectively. The elevated levels of macrophage antigen, angiotensin II type1 receptor, and lipid accumulation were decreased in both the liver and aorta tissues in the aspirintreated group. In conclusion, aspirin can systemically and simultaneously ameliorate NAFLD and atherosclerosis by inhibiting lipid biosynthesis and inflammation and by elevating catabolic metabolism through the activation of the PPARδ-AMPK-PGC-1α pathway. Furthermore, aspirin may normalize atherosclerosis and NAFLD by modulating the mannose receptor and CCR2 in macrophages.

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C1q/TNF-Related Protein-9 Ameliorates Ox-LDL-Induced Endothelial Dysfunction via PGC-1α/AMPK-Mediated Antioxidant Enzyme Induction

Cited by 40 publications

References 63 publications

Notoginsenoside R1 Protects HUVEC Against Oxidized Low Density Lipoprotein (Ox-LDL)-Induced Atherogenic Response via Down-Regulating miR-132

Notoginsenoside R1 Protects HUVEC Against Oxidized Low Density Lipoprotein (Ox-LDL)-Induced Atherogenic Response via Down-Regulating miR-132

C1q/TNF‐related protein 9: A novel therapeutic target in ischemic stroke?

Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPARδ-AMPK-PGC-1αPathway in Dyslipidemic Conditions

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