Innate immunity: involvement of new neuropeptides

Metz‐Boutigue, Marie‐Hélène; Kieffer, Anne-Estelle; Goumon, Yannick; Aunis, Dominique

doi:10.1016/j.tim.2003.10.001

Cited by 65 publications

(48 citation statements)

References 58 publications

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“…calcium channel; myocardial contractility; peptide hormones; endothelial cell CHROMOGRANIN A (CgA) and chromogranin B have long been proposed to control the physiological process of secretory granule formation because of their pH-, Ca 2ϩ -, and catecholamine-dependent aggregation properties (18). In particular, it has been suggested that the 49-kDa acidic protein CgA, co-stored and co-released in the secretory granules of the chromaffin cells, together with catecholamines and other neuromodulators, acts as a prohormone, giving rise to peptides such as vasostatins (VSs), chromacin, pancreastatin, WE-14, catestatin, and parastatin, which are involved in homeostatic processes, including tissue assembly and repair, inflammatory responses, and the first line of defense against invading microorganisms (18,23).…”

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confidence: 99%

Endothelium-derived nitric oxide mediates the antiadrenergic effect of human vasostatin-1 in rat ventricular myocardium

Gallo

Levi²,

Ramella³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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G. Endothelium-derived nitric oxide mediates the antiadrenergic effect of human vasostatin-1 in rat ventricular myocardium. Am J Physiol Heart Circ Physiol 292: H2906 -H2912, 2007. First published February 9, 2007 doi:10.1152/ajpheart.01253.2006 are vasoactive peptides derived from chromogranin A (CgA), a protein contained in secretory granules of chromaffin and other cells. The negative inotropic effect and the reduction of isoproterenol (Iso)-dependent inotropism induced by VSs in the heart suggest that they have an antiadrenergic function. However, further investigation of the mechanisms of action of VSs is needed. The aim of the present study was to define the signaling pathways activated by VS-1 in mammalian ventricular myocardium and cultured endothelial cells that lead to the modulation of cardiac contractility. Ca 2ϩ and nitric oxide (NO) fluorometric confocal imaging was used to study the effects induced by recombinant human VS-1 [STA-CgA-(1-76)] on contractile force, L-type Ca 2ϩ current, and Ca 2ϩ transients under basal conditions and after ␤-adrenergic stimulation in rat papillary muscles and ventricular cells and the effects on intracellular Ca 2ϩ concentration and NO production in cultured bovine aortic endothelial (BAE-1) cells. VS-1 had no effect on basal contractility of papillary muscle, but the effect of Iso stimulation was reduced by 27%. Removal of endocardial endothelium and inhibition of NO synthesis and phosphatidylinositol 3-kinase (PI3K) activity abolished the antiadrenergic effect of VS-1 on papillary muscle. In cardiomyocytes, 10 nM VS-1 was ineffective on basal and Iso (1 M)-stimulated L-type Ca 2ϩ current and Ca 2ϩ transients. In BAE-1 cells, VS-1 induced a Ca 2ϩ -independent increase in NO production that was blocked by the PI3K inhibitor wortmannin. Our results suggest that the antiadrenergic effect of VS-1 is mainly due to a PI3K-dependent NO release by endothelial cells, rather than a direct action on cardiomyocytes. calcium channel; myocardial contractility; peptide hormones; endothelial cell CHROMOGRANIN A (CgA) and chromogranin B have long been proposed to control the physiological process of secretory granule formation because of their pH-, Ca 2ϩ -, and catecholamine-dependent aggregation properties (18).

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mentioning

confidence: 99%

Endothelium-derived nitric oxide mediates the antiadrenergic effect of human vasostatin-1 in rat ventricular myocardium

Gallo

Levi²,

Ramella³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…Chromogranins are released in mammals during stress from the adrenal medulla, along with the adrenaline [36,37]. Our data indicate that D. rerio chromogranins are relatively different from those of tetrapods [38,39], as, although the identity with amphibians and mammals is high in the C-terminal region of the peptide (60-70%), in other regions, the identity is lower than 14-30%.…”

Section: Discussionmentioning

confidence: 69%

Antimicrobial Peptides Are Expressed during Early Development of Zebrafish (Danio rerio) and Are Inducible by Immune Challenge

Caccia

Agnello

Ceci

et al. 2017

Fishes

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Antimicrobial peptides (AMPS) are ancestral components in the evolution of immunity from protozoans to metazoans. Their expression can be constitutive or inducible by infectious challenge. Although characterized in detail in their structure and activity, the temporal and spatial expression of AMPS during vertebrate embryogenesis is still poorly understood. In the present study, we identified selected AMPs in zebrafish, and characterized their expression during early development, and upon experimental immune challenge in adult animals, with the goal of establishing this genetically-tractable model system for further AMP studies. By mining available genomic databases, zebrafish AMP sequences homologous to AMPs from other vertebrates were selected for further study. These included parasin I and its enzyme cathepsin D, β-defensin (DB1), liver-expressed antimicrobial peptide 2 (LEAP2), bactericidal permeability-increasing protein (BPI), and chromogranin-A and -B (CgA and CgB). Specific primers were designed for RT-PCR amplification of each AMP gene of interest and amplicons between 242 bp and 504 bp were obtained from RNA extracted from adult zebrafish. Sequencing of the amplicons and alignment of their deduced amino acid sequences with those from AMPs from other vertebrate species confirmed their identity. The temporal expression of AMPs was investigated by RT-PCR analysis in fertilized oocytes, embryos, and adult individuals. Parasin I and chatepsin D transcripts were detectable immediately after fertilization, while the transcripts for CgA and CgB became evident starting at 48 h post fertilization. Mature transcripts of LEAP2 and DB1 were detectable only in the adult zebrafish, while BPI transcripts were detectable starting from the 12th day post fertilization. To explore the possible upregulation of AMP expression by infectious challenge, experiments were carried out in adult zebrafish by intraperitoneal injection of a cocktail of lipopolysaccharide and lipoteichoic acid. Except for CgA and CgB, amplicons corresponding to all tested AMPs showed stronger signals in the experimental animals as compared to the unchallenged controls. This study provided information on the early expression of AMPs in zebrafish from ontogeny to adulthood and their inducibility by microbials. This information could be useful to actuate new prophylactic strategies as an alternative to the use of antibiotics in culture.

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“…The plasma concentration of the chromogranin A peptide VIF is in the same range of other chromogranin A peptides such as vasostatin-I. 36,37 The plasma concentration of VIF was increased in patients suffering from either CKD or heart failure. This agrees well with reports showing that the plasma concentration of its precursor, chromogranin A, is increased in patients suffering from heart failure and renal failure.…”

Section: Discussionmentioning

confidence: 95%

Identification of the Vasoconstriction-Inhibiting Factor (VIF), a Potent Endogenous Cofactor of Angiotensin II Acting on the Angiotensin II Type 2 Receptor

et al. 2015

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T he renin-angiotensin system and especially the angiotensin peptides play a central role in the pathophysiology of cardiovascular diseases.1,2 Angiotensin peptides are known to play major roles in regulation of the vascular tone and are strongly involved in the pathophysiology of both chronic kidney disease (CKD) 3 and heart failure. 4 The vasoregulatory effects of the angiotensin peptides are mediated by the angiotensin II (Ang-II) type 1 receptor (AT1) receptor, Ang-II type 2 receptor (AT2) receptor, and Mas receptor. Most of the vasoconstrictive effects of angiotensin peptides are mediated by AT1, which is widely distributed in all organs, including adrenal glands, kidney, heart, and vasculature (see Mehta and Griendling 5 for a review). Activation of the AT2 by angiotensin peptides results in vasodilation, nitric oxide release, and Background-The renin-angiotensin system and especially the angiotensin peptides play a central role in blood pressure regulation. Here, we hypothesize that an as-yet unknown peptide is involved in the action of angiotensin II modulating the vasoregulatory effects as a cofactor. Methods and Results-The peptide with vasodilatory properties was isolated from adrenal glands chromatographically.The effects of this peptide were evaluated in vitro and in vivo, and the receptor affinity was analyzed. The plasma concentration in humans was quantified in patients with chronic kidney disease, patients with heart failure, and healthy control subjects. The amino acid sequence of the peptide from bovine adrenal glands was HSSYEDELSEVL EKPNDQAE PKEVTEEVSSKDAAE, which is a degradation product of chromogranin A. The sequence of the peptide isolated from human plasma was HSGFEDELSEVLENQSSQAELKEAVEEPSSKDVME. Both peptides diminished significantly the vasoconstrictive effect of angiotensin II in vitro. Therefore, we named the peptide vasoconstriction-inhibiting factor (VIF). The vasoregulatory effects of VIF are mediated by the angiotensin II type 2 receptor. VIF impairs angiotensin II-induced phosphorylation of the p38 mitogen-activated protein kinase pathway but not of extracellular-regulated kinase 1/2. The vasodilatory effects were confirmed in vivo. The plasma concentration was significantly increased in renal patients and patients with heart failure. Conclusions-VIF is a vasoregulatory peptide that modulates the vasoconstrictive effects of angiotensin II by acting on the angiotensin II type 2 receptor. It is likely that the increase in VIF may serve as a counterregulatory effect to defend against hypertension. The identification of this target may help us to understand the pathophysiology of renal and heart failure and may form a basis for the development of new strategies for the prevention and treatment of cardiovascular disease. inhibition of proliferation and growth. 6,7 The activation of the Mas receptor by angiotensin peptides counteracted many effects of the AT1 receptor such as vasoconstriction. [8][9][10] Among these angiotensin peptides, the physiological and pathophysiological eff...

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Innate immunity: involvement of new neuropeptides

Cited by 65 publications

References 58 publications

Endothelium-derived nitric oxide mediates the antiadrenergic effect of human vasostatin-1 in rat ventricular myocardium

Endothelium-derived nitric oxide mediates the antiadrenergic effect of human vasostatin-1 in rat ventricular myocardium

Antimicrobial Peptides Are Expressed during Early Development of Zebrafish (Danio rerio) and Are Inducible by Immune Challenge

Identification of the Vasoconstriction-Inhibiting Factor (VIF), a Potent Endogenous Cofactor of Angiotensin II Acting on the Angiotensin II Type 2 Receptor

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