CTRP9 enhances carotid plaque stability by reducing pro-inflammatory cytokines in macrophages

Li, Jun; Zhang, Peng; Li, Tingting; Liu, Yawei; Zhu, Qing; Chen, Tongshuai; Liu, Tianjiao; Huang, Chengmin; Zhang, Jianning; Zhang, Yun; Guo, Yuan

doi:10.1016/j.bbrc.2015.02.054

Cited by 52 publications

(39 citation statements)

References 29 publications

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“…Previous experimental studies in mice consistently demonstrated the beneficial effects of CTRP9 on vascular endothelial function [14], vascular smooth muscle cell proliferation [13], and the profile of inflammatory cytokines in macrophages [28, 29]. Several studies have investigated the association of CTRP9 with cardiovascular risk factors in human subjects [15, 16, 18], whereas only two reports have shown the association of CTRP9 with atherosclerosis [18] or cardiovascular disease [16].…”

Section: Discussionmentioning

confidence: 99%

Plasma C1q/TNF-Related Protein-9 Levels Are Associated with Atherosclerosis in Patients with Type 2 Diabetes without Renal Dysfunction

Asada

Morioka

Yamazaki

et al. 2016

Journal of Diabetes Research

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Aim. C1q/tumor necrosis factor-related protein-9 (CTRP9), a paralog of adiponectin, is expressed in adipose tissue. CTRP9 exerts protective effects against obesity and atherosclerosis in rodents. We investigated the association between plasma CTRP9 levels and atherosclerosis in patients with type 2 diabetes. Methods. We included 419 patients with type 2 diabetes, 161 of whom had chronic kidney disease (CKD). Fasting plasma CTRP9 and total adiponectin levels were measured with enzyme-linked immunosorbent assay. The intima-media thickness (IMT) of the common carotid artery was measured with ultrasonography. Results. Plasma CTRP9 levels were higher in the CKD group than in the non-CKD group. Plasma CTRP9 levels were positively correlated with carotid IMT in the non-CKD group. Multivariate analyses revealed that plasma CTRP9 levels were positively associated with carotid IMT in the non-CKD group, independent of age, sex, body mass index, adiponectin, and other cardiovascular risk factors. However, plasma CTRP9 levels were not associated with carotid IMT in the CKD group. Conclusion. Plasma CTRP9 levels are associated with atherosclerosis in diabetic patients without CKD, independently of obesity, adiponectin, and traditional cardiovascular risk factors. This study indicates a potential role of CTRP9 in atherosclerosis progression in human type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Plasma C1q/TNF-Related Protein-9 Levels Are Associated with Atherosclerosis in Patients with Type 2 Diabetes without Renal Dysfunction

Asada

Morioka

Yamazaki

et al. 2016

Journal of Diabetes Research

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“…The abundance of each component was evaluated as percent of the vascular intima area. The vulnerable index was calculated as follows: the relative positive staining areas of (macrophages% + lipid%)/the relative positive staining areas of (SMCs% + collagen%) [29]. …”

Section: Methodsmentioning

confidence: 99%

Myeloperoxidase-oxidized high density lipoprotein impairs atherosclerotic plaque stability by inhibiting smooth muscle cell migration

Zhou¹,

Zu²,

Chen

et al. 2017

Lipids Health Dis

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BackgroundHigh density lipoprotein (HDL) has been proved to be a protective factor for coronary heart disease. Notably, HDL in atherosclerotic plaques can be nitrated (NO2-oxHDL) and chlorinated (Cl-oxHDL) by myeloperoxidase (MPO), likely compromising its cardiovascular protective effects.MethodHere we determined the effects of NO2-oxHDL and Cl-oxHDL on SMC migration using wound healing and transwell assays, proliferation using MTT and BrdU assays, and apoptosis using Annexin-V assay in vitro, as well as on atherosclerotic plaque stability in vivo using a coratid artery collar implantation mice model.ResultsOur results showed that native HDL promoted SMC proliferation and migration, whereas NO2-oxHDL and Cl-oxHDL inhibited SMC migration and reduced capacity of stimulating SMC proliferation as well as migration, respectively. OxHDL had no significant influence on SMC apoptosis. In addition, we found that ERK1/2-phosphorylation was significantly lower when SMCs were incubated with NO2-oxHDL and Cl-oxHDL. Furthermore, transwell experiments showed that differences between native HDL, NO2-oxHDL and Cl-oxHDL was abolished after PD98059 (MAPK kinase inhibitor) treatment. In aortic SMCs from scavenger receptor BI (SR-BI) deficient mice, differences between migration of native HDL, NO2-oxHDL and Cl-oxHDL treated SMCs vanished, indicating SR-BI’s possible role in HDL-associated SMC migration. Importantly, NO2-oxHDL and Cl-oxHDL induced neointima formation and reduced SMC positive staining cells in atherosclerotic plaque, resulting in elevated vulnerable index of atherosclerotic plaque.ConclusionThese findings implicate MPO-catalyzed oxidization of HDL may contribute to atherosclerotic plaque instability by inhibiting SMC proliferation and migration through MAPK-ERK pathway which was dependent on SR-BI.Electronic supplementary materialThe online version of this article (doi:10.1186/s12944-016-0388-z) contains supplementary material, which is available to authorized users.

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“…50 Furthermore, administration of CTRP9 by the lentiviral vector system reduced the macrophage and lipid content of carotid plaques in ApoE-KO mice, indicating CTRP9 may be an antiatherogenic factor. 51 Taken together, it is likely CTRP9 possesses vascular protective effects, but future studies using transgenic animal models are necessary to dissect the role endogenous CTRP9 plays in vascular disease.…”

Section: Role Of Adipokines In Vascular Diseasesmentioning

confidence: 99%

Role of Adipokines in Cardiovascular Disease

Lau

Ohashi

Wang

et al. 2017

Circ J

142

101

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Cardiovascular disease (CVD) is the greatest cause of death, accounting for nearly one-third of all deaths worldwide. The increase in obesity rates over 3 decades is widespread and threatens the public health in both developed and developing countries. Obesity, the excessive accumulation of visceral fat, causes the clustering of metabolic disorders, such as type 2 diabetes, dyslipidemia, and hypertension, culminating in the development of CVD. Adipose tissue is not only an energy storage organ, but an active endocrine tissue producing various biologically active proteins known as adipokines. Since leptin, a central regulator of food intake and energy expenditure, was demonstrated to be an adipose-specific adipokine, attention has focused on the identification and characterization of unknown adipokines to clarify the mechanisms underlying obesity-related disorders. Numerous adipokines have been identified in the past 2 decades; most adipokines are upregulated in the obese state. Adipokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and resistin are pro-inflammatory, and exacerbate various metabolic and cardiovascular diseases. However, a small number of adipokines, including adiponectin, are decreased by obesity, and generally exhibit antiinflammatory properties and protective functions against obesity-related diseases. Collectively, an imbalance in the production of pro-and antiinflammatory adipokines in the obese condition results in multiple complications. In this review, we focus on the pathophysiologic roles of adipokines with cardiovascular protective properties.

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CTRP9 enhances carotid plaque stability by reducing pro-inflammatory cytokines in macrophages

Cited by 52 publications

References 29 publications

Plasma C1q/TNF-Related Protein-9 Levels Are Associated with Atherosclerosis in Patients with Type 2 Diabetes without Renal Dysfunction

Plasma C1q/TNF-Related Protein-9 Levels Are Associated with Atherosclerosis in Patients with Type 2 Diabetes without Renal Dysfunction

Myeloperoxidase-oxidized high density lipoprotein impairs atherosclerotic plaque stability by inhibiting smooth muscle cell migration

Role of Adipokines in Cardiovascular Disease

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