Catestatin peptide of chromogranin A as a potential new target for several risk factors management in the course of metabolic syndrome

Bourebaba, Yasmina; Mularczyk, Malwina; Marycz, Krzyzstof; Bourebaba, Lynda

doi:10.1016/j.biopha.2020.111113

Cited by 25 publications

(15 citation statements)

References 164 publications

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“…These anti-atherosclerotic effects are attributed to the molecular and cellular protective effects against atherosclerosis, as described above. Catestatin also attenuates insulin resistance, hypertension, and obesity in murine models, and contributes to the prevention of metabolic syndrome [ 116 ]. CgA-knockout mice reveal hypertension, high plasma catecholamine and adiponectin levels, and lower interleukin-6 and lipid levels compared with wild type mice [ 117 ].…”

Section: Atherosclerosismentioning

confidence: 99%

The Emerging Roles of Chromogranins and Derived Polypeptides in Atherosclerosis, Diabetes, and Coronary Heart Disease

Watanabe

2021

IJMS

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Chromogranin A (CgA), B (CgB), and C (CgC), the family members of the granin glycoproteins, are associated with diabetes. These proteins are abundantly expressed in neurons, endocrine, and neuroendocrine cells. They are also present in other areas of the body. Patients with diabetic retinopathy have higher levels of CgA, CgB, and CgC in the vitreous humor. In addition, type 1 diabetic patients have high CgA and low CgB levels in the circulating blood. Plasma CgA levels are increased in patients with hypertension, coronary heart disease, and heart failure. CgA is the precursor to several functional peptides, including catestatin, vasostatin-1, vasostatin-2, pancreastatin, chromofungin, and many others. Catestatin, vasostain-1, and vasostatin-2 suppress the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 in human vascular endothelial cells. Catestatin and vasostatin-1 suppress oxidized low-density lipoprotein-induced foam cell formation in human macrophages. Catestatin and vasostatin-2, but not vasostatin-1, suppress the proliferation and these three peptides suppress the migration in human vascular smooth muscles. Chronic infusion of catestatin, vasostatin-1, or vasostatin-2 suppresses the development of atherosclerosis of the aorta in apolipoprotein E-deficient mice. Catestatin, vasostatin-1, vasostatin-2, and chromofungin protect ischemia/reperfusion-induced myocardial dysfunction in rats. Since pancreastatin inhibits insulin secretion from pancreatic β-cells, and regulates glucose metabolism in liver and adipose tissues, pancreastatin inhibitor peptide-8 (PSTi8) improves insulin resistance and glucose homeostasis. Catestatin stimulates therapeutic angiogenesis in the mouse hind limb ischemia model. Gene therapy with secretoneurin, a CgC-derived peptide, stimulates postischemic neovascularization in apolipoprotein E-deficient mice and streptozotocin-induced diabetic mice, and improves diabetic neuropathy in db/db mice. Therefore, CgA is a biomarker for atherosclerosis, diabetes, hypertension, and coronary heart disease. CgA- and CgC--derived polypeptides provide the therapeutic target for atherosclerosis and ischemia-induced tissue damages. PSTi8 is useful in the treatment of diabetes.

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Section: Atherosclerosismentioning

confidence: 99%

The Emerging Roles of Chromogranins and Derived Polypeptides in Atherosclerosis, Diabetes, and Coronary Heart Disease

Watanabe

2021

IJMS

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“…CST-KO mice are associated with an altered gut microbiota composition, and richness (Figure 1 and González-Dávila et al 2021 ) . A major parallel between the CST-KO microbiota profiles and the WT mice that received the FMT from the CST-KO (WT FMT-CST-KO ) encompassed a reduction of Clostridia and Akkermansia , which has been previously linked to metabolic disorders and insulin resistance (Schneeberger et al, 2015; Zhou et al, 2021), a CST-KO related phenotype (Bourebaba et al, 2021) as well as a prominent increase in the Proteobacteria population, all of which have been found previously to be indicative for active IBD states (Earley et al, 2019; Glassner et al, 2020). In contrast, CST-KO that received the FMT from the WT mice (CST-KO FMT-WT ) encompassed an increase in richness and a notable reduction of Staphylococcus , as well as an increase in the butyrate-producing Intestinimonas (Figure 1).…”

Section: Discussionmentioning

confidence: 99%

Gut microbiota transplantation drives the adoptive transfer of colonic genotype-phenotype characteristics between mice lacking catestatin and their wild type counterparts

González-Dávila

Schwalbe

Danewalia

et al. 2022

Preprint

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The gut microbiota is in continuous interaction with the intestinal mucosa via metabolic, neuro-immunological, and neuroendocrine pathways. Disruption in levels of antimicrobial peptides produced by the enteroendocrine cells, such as catestatin, has been associated with changes in the gut microbiota and imbalance in intestinal homeostasis. However, whether the changes in the gut microbiota have a causational role in intestinal dyshomeostasis has remained elusive. To this end, we performed reciprocal fecal microbial transplantation in wild-type mice and mice with a knockout in the catestatin coding region of the chromogranin-A gene (CST-KO mice). Combined microbiota phylogenetic profiling, RNA sequencing, and transmission electron microscopy were employed. Fecal microbiota transplantation from mice deficient in catestatin (CST-KO) to microbiota-depleted wild-type mice induced transcriptional and physiological features characteristic of a distorted colon in the recipient animals, including impairment in tight junctions, as well as an increased collagen area fraction indicating colonic fibrosis. In contrast, fecal microbiota transplantation from wild-type mice to microbiota-depleted CST-KO mice reduced collagen fibrotic area, restored disrupted tight junction morphology, and altered fatty acid metabolism in recipient CST-KO mice. This study provides a comprehensive overview of the murine metabolic- and immune-related cellular pathways and processes that are co-mediated by the fecal microbiota transplantation and supports a prominent role for the gut microbiota in the colonic distortion associated with the lack of catestatin in mice. Overall, the data show that the gut microbiota may play a causal role in the development of features of intestinal inflammation and metabolic disorders, known to be associated with altered levels of catestatin and may, thus, provide a tractable target in the treatment and prevention of these disorders.

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“…Apart from the well-established role of catestatin in CVD, the data indicate that catestatin is linked to inflammatory and metabolic syndrome diseases and can be a novel regulator of insulin and lipid levels [ 77 ]. In an obese mouse model it was demonstrated that catestatin infusion leads to body weight reduction mediated by the inhibition of alpha2-adrenergic receptor signaling and the enhancement of leptin receptor signaling [ 78 ].…”

Section: Role Of Catestatin In Various Cardiovascular Disordersmentioning

confidence: 99%

Catestatin as a Biomarker of Cardiovascular Diseases: A Clinical Perspective

et al. 2021

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Accounting for almost one-third of the global mortality, cardiovascular diseases (CVDs) represent a major global health issue. Emerging data suggest that most of the well-established mechanistic explanations regarding the cardiovascular pathophysiology are flawed, and cannot fully explain the progression and long-term effects of these diseases. On the other hand, dysregulation of the sympathetic nervous system (SNS) has emerged as an important player in the pathophysiology of CVDs. Even though upregulated SNS activity is an essential compensatory response to various stress conditions, in the long term, it becomes a major contributor to both cardiac dysfunction and vascular damage. Despite the fact that the importance of SNS hyperactivity in the setting of CVDs has been well-appreciated, its exact quantification and clinical application in either diagnostics or therapy of CVDs is still out of reach. Nevertheless, in recent years a number of novel laboratory biomarkers implicated in the pathophysiology of SNS activation have been explored. Specifically, in this review, we aimed to discuss the role of catestatin, a potent physiological inhibitor of catecholamine spillover that offers cardioprotective effects. Limited data indicate that catestatin could also be a reliable indirect marker of SNS activity and it is likely that high CST levels reflect advanced CV disease burden. Consequently, large-scale studies are required to validate these observations in the upcoming future.

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Catestatin peptide of chromogranin A as a potential new target for several risk factors management in the course of metabolic syndrome

Cited by 25 publications

References 164 publications

The Emerging Roles of Chromogranins and Derived Polypeptides in Atherosclerosis, Diabetes, and Coronary Heart Disease

The Emerging Roles of Chromogranins and Derived Polypeptides in Atherosclerosis, Diabetes, and Coronary Heart Disease

Gut microbiota transplantation drives the adoptive transfer of colonic genotype-phenotype characteristics between mice lacking catestatin and their wild type counterparts

Catestatin as a Biomarker of Cardiovascular Diseases: A Clinical Perspective

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