Plasma Catestatin in Patients with Acute Coronary Syndrome

Xu, Weiting; Yu, Haiyi; Wu, Hubing; Li, Siheng; Chen, Baoxia; Gao, Wei

doi:10.1159/000448987

Cited by 19 publications

(16 citation statements)

References 24 publications

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“…24 Conflicting results have been recently reported by increased or decreased plasma levels of catestatin in patients with coronary artery disease (CAD). [25][26][27][28][29] Therefore, the precise effects of catestatin on arteriosclerosis have not yet been elucidated.…”

Section: Introductionmentioning

confidence: 99%

Catestatin Prevents Macrophage-Driven Atherosclerosis but Not Arterial Injury–Induced Neointimal Hyperplasia

et al. 2018

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Catestatin, a catecholamine-release inhibitory peptide, has multiple cardiovascular activities. Conflicting results have been recently reported by increased or decreased plasma levels of catestatin in patients with coronary artery disease (CAD). However, there have been no previous reports regarding the effects of catestatin on arteriosclerosis. This study evaluated the vasoprotective effects of catestatin on human macrophages, human aortic smooth muscle cells (HASMCs) and human umbilical vein endothelial cells (HUVECs) in vitro, and aortic atherosclerosis and wire injury-induced femoral artery neointimal hyperplasia in apolipoprotein E-deficient (ApoE) mice fed with a high-cholesterol diet. Histological expression of catestatin in coronary artery lesions and its plasma level were compared between CAD and non-CAD patients. Catestatin was abundantly expressed in cultured human monocytes, macrophages, HASMCs and HUVECs. Catestatin significantly suppressed lipopolysaccharide-induced upregulation of tumour necrosis factor-α, vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 in HUVECs. Catestatin significantly suppressed inflammatory responses and oxidized low-density lipoprotein-induced foam cell formation associated with acyl-CoA:cholesterol acyltransferase-1 downregulation and ATP-binding cassette transporter A1 upregulation in human macrophages. Catestatin significantly suppressed migration, proliferation and collagen-1 expression without inducing apoptosis, and increased elastin and fibronectin expression in HASMCs. Administration of catestatin into ApoE mice significantly retarded entire aortic atherosclerotic lesions with declined contents of macrophages, SMCs and collagen fibres in atheromatous plaques, but not the femoral artery injury-induced neointimal hyperplasia. In CAD patients, catestatin levels were significantly decreased in plasma but increased in coronary atheromatous plaques. This study provided the first evidence that catestatin could prevent macrophage-driven atherosclerosis, but not SMC-derived neointimal hyperplasia after vascular injury.

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Section: Introductionmentioning

confidence: 99%

Catestatin Prevents Macrophage-Driven Atherosclerosis but Not Arterial Injury–Induced Neointimal Hyperplasia

et al. 2018

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“…In particular, we hypothesized that in adult rat cardiomyocytes Cts could increase the first step in cardiac glucose metabolism and glucose uptake mediated by the Glut4 transporters, by inducing Glut4 translocation to the plasma membrane. We used 10 nM Catestatin, a mildly high concentration with respect to the plasmatic level measured in healthy subject [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Catestatin Induces Glucose Uptake and GLUT4 Trafficking in Adult Rat Cardiomyocytes

Gallo

Femminò

Antoniotti

et al. 2018

BioMed Research International

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Catestatin is a cationic and hydrophobic peptide derived from the enzymatic cleavage of the prohormone Chromogranin A. Initially identified as a potent endogenous nicotinic–cholinergic antagonist, Catestatin has recently been shown to act as a novel regulator of cardiac function and blood pressure and as a cardioprotective agent in both pre- and postconditioning through AKT-dependent mechanisms. The aim of this study is to investigate the potential role of Catestatin also on cardiac metabolism modulation, particularly on cardiomyocytes glucose uptake. Experiments were performed on isolated adult rat cardiomyocytes. Glucose uptake was assessed by fluorescent glucose incubation and confocal microscope analysis. Glut4 plasma membrane translocation was studied by immunofluorescence experiments and evaluation of the ratio peripheral vs internal Glut4 staining. Furthermore, we performed immunoblot experiments to investigate the involvement of the intracellular pathway AKT/AS160 in the Catestatin dependent Glut4 trafficking. Our results show that 10 nM Catestatin induces a significant increase in the fluorescent glucose uptake, comparable to that exerted by 100 nM Insulin. Moreover, Catestatin stimulates Glut4 translocation to plasma membrane and both AKT and AS160 phosphorylation. All these effects were inhibited by Wortmannin. On the whole, we show for the first time that Catestatin is able to modulate cardiac glucose metabolism, by inducing an increase in glucose uptake through Glut4 translocation to the plasma membrane and that this mechanism is mediated by the AKT/AS160 intracellular pathway.

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“…Interestingly, those with increased plasma catestatin and BNP were at highest risk of all-cause and cardiac death. Xu et al, studied patients with acute ST-segment elevation myocardial infarction (STEMI, n=46), unstable angina pectoris (n=89), and no coronary artery disease (n=35) [186]. They found that plasma catestatin levels were lower in the STEMI and unstable angina groups compared to controls.…”

Section: 0 Additional Neuropeptidesmentioning

confidence: 99%

The role of neuropeptides in adverse myocardial remodeling and heart failure

Widiapradja

Chunduri

Levick

2017

Cell. Mol. Life Sci.

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In addition to traditional neurotransmitters of the sympathetic and parasympathetic nervous systems, the heart also contains numerous neuropeptides. These neuropeptides not only modulate the effects of neurotransmitters, but also have independent effects on cardiac function. While in most cases the physiological actions of these neuropeptides are well defined, their contributions to cardiac pathology are less appreciated. Some neuropeptides are cardioprotective, some promote adverse cardiac remodeling and heart failure, and in the case of others their functions are unclear. Some have both cardioprotective and adverse effects depending on the specific cardiac pathology and progression of that pathology. In this review, we briefly describe the actions of several neuropeptides on normal cardiac physiology, before describing in more detail their role in adverse cardiac remodeling and heart failure. It is our goal to bring more focus toward understanding the contribution of neuropeptides to the pathogenesis of heart failure, and to consider them as potential therapeutic targets.

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Plasma Catestatin in Patients with Acute Coronary Syndrome

Cited by 19 publications

References 24 publications

Catestatin Prevents Macrophage-Driven Atherosclerosis but Not Arterial Injury–Induced Neointimal Hyperplasia

Catestatin Prevents Macrophage-Driven Atherosclerosis but Not Arterial Injury–Induced Neointimal Hyperplasia

Catestatin Induces Glucose Uptake and GLUT4 Trafficking in Adult Rat Cardiomyocytes

The role of neuropeptides in adverse myocardial remodeling and heart failure

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