Associations of serum salusin-alpha levels with atherosclerosis and left ventricular diastolic dysfunction in essential hypertension

Ti, Yun; Wang, F; Zh, Wang; Xl, Wang; Zhang, W; Zhang, Y; Pl, Bu

doi:10.1038/jhh.2011.71

Cited by 23 publications

(24 citation statements)

References 27 publications

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“…Our data and others have demonstrated that decreased levels of serum salusin- α are associated with carotid atherosclerosis and cardiac dysfunction in patients with essential hypertension and with renal dysfunction in patients with chronic kidney diseases [45–47]. We recently suggested the possible mechanisms responsible for decreased production of salusin- α in atherosclerotic lesions.…”

Section: Linkage Of Salusins With Atherosclerotic Cardiovascular supporting

confidence: 54%

Salusins: Potential Use as a Biomarker for Atherosclerotic Cardiovascular Diseases

Sato

Watanabe

Itoh

et al. 2013

International Journal of Hypertension

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Human salusin-α and salusin-β are related peptides produced from prosalusin. Bolus injection of salusin-β into rats induces more profound hypotension and bradycardia than salusin-α. Central administration of salusin-β increases blood pressure via release of norepinephrine and arginine-vasopressin. Circulating levels of salusin-α and salusin-β are lower in patients with essential hypertension. Salusin-β exerts more potent mitogenic effects on human vascular smooth muscle cells (VSMCs) and fibroblasts than salusin-α. Salusin-β accelerates inflammatory responses in human endothelial cells and monocyte-endothelial adhesion. Human macrophage foam cell formation is stimulated by salusin-β but suppressed by salusin-α. Chronic salusin-β infusion into apolipoprotein E-deficient mice enhances atherosclerotic lesions; salusin-α infusion reduces lesions. Salusin-β is expressed in proliferative neointimal lesions of porcine coronary arteries after stenting. Salusin-α and salusin-β immunoreactivity have been detected in human coronary atherosclerotic plaques, with dominance of salusin-β in macrophage foam cells, VSMCs, and fibroblasts. Circulating salusin-β levels increase and salusin-α levels decrease in patients with coronary artery disease. These findings suggest that salusin-β and salusin-α may contribute to proatherogenesis and antiatherogenesis, respectively. Increased salusin-β and/or decreased salusin-α levels in circulating blood and vascular tissue are closely linked with atherosclerosis. Salusin-α and salusin-β could be candidate biomarkers and therapeutic targets for atherosclerotic cardiovascular diseases.

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Section: Linkage Of Salusins With Atherosclerotic Cardiovascular supporting

confidence: 54%

Salusins: Potential Use as a Biomarker for Atherosclerotic Cardiovascular Diseases

Sato

Watanabe

Itoh

et al. 2013

International Journal of Hypertension

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“…Therefore, elevated peripheral salusin-β levels could represent the amount of peptide secreted by macrophages in response to vascular inflammatory processes. Recent studies have reported that serum salusin-α levels, which possess contrasting antiatherosclerotic activity by suppressing macrophage foam cell formation, are lower in patients with coronary artery disease, hypertension, and renal failure than in healthy controls, and the magnitude of decrease in serum salusin-α appears pronounced as atherosclerosis advances [7,15,17,21]. Therefore, salusin-α has been proposed as a candidate biomarker for atherosclerotic and cardiovascular diseases in humans [18,19].…”

Section: Discussionmentioning

confidence: 99%

Circulating Levels of Human salusin-β,a Potent Hemodynamic and Atherogenesis Regulator

et al. 2013

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Using bioinformatics analysis, we previously identified salusin-β, an endogenous bioactive peptide with diverse physiological activities. Salusin-β is abundantly expressed in the neuroendocrine system and in systemic endocrine cells/macrophages. Salusin-β acutely regulates hemodynamics and chronically induces atherosclerosis, but its unique physicochemical characteristics to tightly adhere to all types of plastic and glassware have prevented elucidation of its precise pathophysiological role. To quantitate plasma total salusin-β concentrations, we produced rabbit and chicken polyclonal antibodies against the C- and N-terminal end sequences, circumvented its sticky nature, and successfully established a sandwich enzyme-linked immunosorbent assay (ELISA). Salusin-β was abundantly present in the plasma of healthy volunteers, ranging from 1.9 to 6.6 nmol/L. Reverse phase-high performance liquid chromatography analysis showed that a single immunoreactive salusin-β peak coincided with synthetic authentic salusin-β. Plasma salusin-β concentrations were unaffected by postural changes and by potent vasopressin release stimuli, such as hypertonic saline infusion or smoking. However, salusin-β concentrations showed significant circadian variation; concentrations were high during the daytime and reached the lowest concentrations in the early morning. Plasma salusin-β levels in subjects with diabetes mellitus, coronary artery disease, and cerebrovascular disease showed distinctly higher levels than healthy controls. Patients with panhypopituitarism combined with complete central diabetes insipidus also showed significantly higher plasma salusin-β levels. Therefore, the ELISA system developed in this study will be useful for evaluating circulating total salusin-β levels and for confirming the presence of authentic salusin-β in human plasma. The obtained results suggest a limited contribution of the neuroendocrine system to peripheral total salusin-β concentrations and a role for plasma total salusin-β concentrations as an indicator of systemic vascular diseases.

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“…Moreover, compared with healthy volunteers, patients with coronary artery diseases manifest reduced concentrations of serum salusin-α [6]. Serum salusin-α level is also associated with atherosclerosis and left ventricular diastolic dysfunction in essential hypertension [7], [8]. In addition, our recent study shows that the expression of salusin-β is increased in the vascular tissues of low-density lipoprotein receptor-deficient (LDLR-/-) mice fed on high-fat diets compared with that of C57BL/6 control mice [9].…”

Section: Introductionmentioning

confidence: 99%

Salusin-β Not Salusin-α Promotes Vascular Inflammation in ApoE-Deficient Mice via the I-κBα/NF-κB Pathway

Zhou

Liu

et al. 2014

PLoS ONE

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ObjectiveVascular inflammation plays an important role in the development and progression of atherosclerosis. Recently, salusins (salusin-α and salusin-β) have been reported to be associated wtih atherosclerosis. However, its underlying mechanism remains incompletely known. In this study, we observed the effects of salusins on vascular inflammation in apoE-deficient (apoE-/-) mice.Methods and ResultsSix-week old male apoE-/- mice were infused with salusin-α, salusin-β or vehicle for 8 weeks via osmotic mini-pumps. Our results showed that apoE-/- mice receiving vehicle alone developed severe atherosclerotic lesions and dyslipidemia, with significantly up-regulated levels of IL-6, TNF-α, VCAM-1 and MCP-1. For apoE-/- mice receiving 8 weeks of salusin-β infusion, the atherosclerotic lesions were markedly aggravated, and the levels of IL-6, TNF-α, VCAM-1 and MCP-1 were substantially increased, despite a similar plasma lipid concentration with that of apoE-/- mice. However, after 8 week-infusion of salusin-α, apoE-/- mice presented significant amelioration in atherosclerotic lesions, along with remarkably up-regulated level of high-density lipoprotein-cholesterol (HDL-C) and down-regulated levels of IL-6 and TNF-α, but without any effect on the expressions of VCAM-1 and MCP-1. Furthermore, the activation of nuclear factor-κB (NF-κB), an important transcription factor essential for inflammatory molecules, and the degradation of I-κBα, an inhibitor of NF-κB, were markedly increased in apoE-/- mice receiving vehicle alone. Treatment with salusin-β not salusin-α could remarkably accelerate the process of NF-κB nuclear translocation and I-κBα degradation.ConclusionSalusin-β, but not salusin-α, promotes vascular inflammation in apoE-deficient mice via the I-κBα/NF-κB pathway. These findings provide further insight into the mechanism of salusins in atherosclerosis and potential targets for the prevention and treatment of atherosclerosis.

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Associations of serum salusin-alpha levels with atherosclerosis and left ventricular diastolic dysfunction in essential hypertension

Cited by 23 publications

References 27 publications

Salusins: Potential Use as a Biomarker for Atherosclerotic Cardiovascular Diseases

Salusins: Potential Use as a Biomarker for Atherosclerotic Cardiovascular Diseases

Circulating Levels of Human salusin-β,a Potent Hemodynamic and Atherogenesis Regulator

Salusin-β Not Salusin-α Promotes Vascular Inflammation in ApoE-Deficient Mice via the I-κBα/NF-κB Pathway

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