Characterization of natural vasostatin‐containing peptides in rat heart

Glattard, Elise; Angelone, Tommaso; Strub, Jean‐Marc; Corti, Angelo; Aunis, Dominique; Tota, Bruno; Metz‐Boutigue, Marie‐Hélène; Goumon, Yannick

doi:10.1111/j.1742-4658.2006.05334.x

Cited by 49 publications

(35 citation statements)

References 70 publications

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“…Additionally, immunohistochemical studies in serial sections from atrial and ventricular regions of rat heart demonstrated localization of CHGA along with the calcium channel alpha 1E subunit in Purkinje fibers of both atrium and ventricle [46]. Consistent with these findings, CHGA-derived vasostatincontaining peptides were identified in rat heart extracts, indicating their role in cardiac physiology by an autocrine/paracrine mechanism [47]. More recently, convincing evidences of production and release of CHGA in human ventricular myocardium were provided by Pieroni et al [48].…”

Section: Introductionsupporting

confidence: 68%

Chromogranin A: a novel susceptibility gene for essential hypertension

Sahu

Sonawane

Mahapatra

2009

Cell. Mol. Life Sci.

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Chromogranin A (CHGA) is ubiquitously expressed in secretory cells of the endocrine, neuroendocrine, and neuronal tissues. Although this protein has long been known as a marker for neuroendocrine tumors, its role in cardiovascular disease states including essential hypertension (EH) has only recently been recognized. It acts as a prohormone giving rise to bioactive peptides such as vasostatin-I (human CHGA(1-76)) and catestatin (human CHGA(352-372)) that exhibit several cardiovascular regulatory functions. CHGA is over-expressed but catestatin is diminished in EH. Moreover, genetic variants in the promoter, catestatin, and 3'-untranslated regions of the human CHGA gene alter autonomic activity and blood pressure. Consistent with these findings, targeted ablation of this gene causes severe arterial hypertension and ventricular hypertrophy in mice. Transgenic expression of the human CHGA gene or exogenous administration of catestatin restores blood pressure in these mice. Thus, the accumulated evidence establishes CHGA as a novel susceptibility gene for EH.

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Section: Introductionsupporting

confidence: 68%

Chromogranin A: a novel susceptibility gene for essential hypertension

Sahu

Sonawane

Mahapatra

2009

Cell. Mol. Life Sci.

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“…Numerous monobasic and dibasic amino acid residues in CgA indicate potential sites for endoproteolytic processing by the prohormone convertases (subtilisin-like and trypsin-like) PC1/3 and PC2 that occur as co-stored components of neurosecretory granules (Seidah and Chretien, 1999), including the myocardial-specific granules (Muth et al, 2004). Four N-terminal CgA-derived peptides (CgA4-113, CgA1-124, CgA1-135 and CgA1-199) have been characterized from rat heart homogenates, which is consistent with cleavage into betagranins, containing the homologous VS-1 motif (Glattard et al, 2006). Thus, the possibility exists that in the eel heart CST, locally generated from intracardiac CgA, participates in the autocrine-paracrine modulation of myocardial performance under both unstimulated and adrenergically stimulated (see below) conditions.…”

Section: Effects Of Cst On Basal Mechanical Performancementioning

confidence: 95%

The catecholamine release-inhibitory peptide catestatin (chromogranin A344-364) modulates myocardial function in fish

Imbrogno

Garofalo

Cerra

et al. 2010

Journal of Experimental Biology

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ISO-and endothelin-1-induced positive inotropism and coronary constriction . Thus, besides its antihypertensive properties, CST is now emerging as a novel cardiac modulator, which would protect the heart against excessive systemic and/or intra-cardiac excitatory stimuli (e.g. catecholamines and endothelin-1). Accepted 4 August 2010 SUMMARY Catestatin (CST), the 21-amino acid, cationic and hydrophobic peptide proteolytically derived from the ubiquitous chromogranin A (CgA), is an endogenous inhibitor of catecholamine release, a potent vasodilator in vivo and an anti-hypertensive agent in mammals, including humans. Recently, we discovered that CST also functions as an important negative modulator of heart performance in frog and rat. To gain an evolutionary perspective on CST cardiotropism in fish, we analysed the influence of bovine CST (CgA 344-364 ) on the eel heart, as well as the eventual species-specific mechanisms of its myocardial action. Experiments were carried out on fresh-water eels (Anguilla anguilla L.) using an electrically paced isolated working heart preparation.

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“…Recent evidence indicates the possible intracardiac production of VS. In fact, several N-terminal fragments containing the VS-1 domain were detected in rat heart extracts (CgA 4-113 , CgA 1-124 , CgA 1-135 and CgA 1-199 ) together with a larger fragment, presumably corresponding to the intact CgA, suggesting an intracardiac cleavage of the precursor (Glattard et al, 2006).…”

Section: Qkkhsgfedelsevlenqssqaelkeaveepsskdvmekrmentioning

confidence: 99%

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Tota

Cerra

Gattuso

2010

Journal of Experimental Biology

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Summary In the past 50 years, extensive evidence has shown the ability of vertebrate cardiac non-neuronal cells to synthesize and release catecholamines (CA). This formed the mindset behind the search for the intrinsic endocrine heart properties, culminating in 1981 with the discovery of the natriuretic peptides (NP). CA and NP, co-existing in the endocrine secretion granules and acting as major cardiovascular regulators in health and disease, have become of great biomedical relevance for their potent diagnostic and therapeutic use. The concept of the endocrine heart was later enriched by the identification of a growing number of cardiac hormonal substances involved in organ modulation under normal and stress-induced conditions. Recently, chromogranin A (CgA), a major constituent of the secretory granules, and its derived cardio-suppressive and antiadrenergic peptides, vasostatin-1 and catestatin, were shown as new players in this framework, functioning as cardiac counter-regulators in ‘zero steady-state error’ homeostasis, particularly under intense excitatory stimuli, e.g. CA-induced myocardial stress. Here, we present evidence for the hypothesis that is gaining support, particularly among human cardiologists. The actions of CA, NP and CgA, we argue, may be viewed as a hallmark of the cardiac capacity to organize ‘whip-brake’ connection-integration processes in spatio-temporal networks. The involvement of the nitric oxide synthase (NOS)/nitric oxide (NO) system in this configuration is discussed. The use of fish and amphibian paradigms will illustrate the ways that incipient endocrine-humoral agents have evolved as components of cardiac molecular loops and important intermediates during evolutionary transitions, or in a distinct phylogenetic lineage, or under stress challenges. This may help to grasp the old evolutionary roots of these intracardiac endocrine/paracrine networks and how they have evolved from relatively less complicated designs. The latter can also be used as an intellectual tool to disentangle the experimental complexity of the mammalian and human endocrine hearts, suggesting future investigational avenues.

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Characterization of natural vasostatin‐containing peptides in rat heart

Cited by 49 publications

References 70 publications

Chromogranin A: a novel susceptibility gene for essential hypertension

Chromogranin A: a novel susceptibility gene for essential hypertension

The catecholamine release-inhibitory peptide catestatin (chromogranin A344-364) modulates myocardial function in fish

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

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