The role of neuropeptides in adverse myocardial remodeling and heart failure

Widiapradja, Alexander; Chunduri, Prasad; Levick, Scott P.

doi:10.1007/s00018-017-2452-x

Cited by 19 publications

(13 citation statements)

References 215 publications

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“…It has been postulated that these differences may be due to high NPY levels only occurring when there is sustained and sufficiently high sympathetic activation (Pedrazzini et al, 2003 ). As recently discussed (Widiapradja et al, 2017 ), it should be noted that there may also be differences between the plasma levels of NPY measured in these studies, and actual cardiac tissue concentrations. A high cardiac output model of heart failure in the rat found high plasma levels but reduced tissue levels in the heart (Callanan et al, 2007 ) although this may be as a result of increased cardiac release of NPY.…”

Section: Neuropeptide Y As An Important Mediator Of Cardiovascular DImentioning

confidence: 74%

The Role of Neuropeptide Y in Cardiovascular Health and Disease

et al. 2018

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Neuropeptide Y (NPY) is an abundant sympathetic co-transmitter, widely found in the central and peripheral nervous systems and with diverse roles in multiple physiological processes. In the cardiovascular system it is found in neurons supplying the vasculature, cardiomyocytes and endocardium, and is involved in physiological processes including vasoconstriction, cardiac remodeling, and angiogenesis. It is increasingly also implicated in cardiovascular disease pathogenesis, including hypertension, atherosclerosis, ischemia/infarction, arrhythmia, and heart failure. This review will focus on the physiological and pathogenic role of NPY in the cardiovascular system. After summarizing the NPY receptors which predominantly mediate cardiovascular actions, along with their signaling pathways, individual disease processes will be considered. A thorough understanding of these roles may allow therapeutic targeting of NPY and its receptors.

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Section: Neuropeptide Y As An Important Mediator Of Cardiovascular DImentioning

confidence: 74%

The Role of Neuropeptide Y in Cardiovascular Health and Disease

et al. 2018

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“…Given the role of SP in cardiovascular disease (Dehlin and Levick, 2014;Widiapradja et al, 2017), we were interested in whether cardiac MCs from diseased hearts were more responsive to SP. Accordingly, we isolated MCs from SHR hearts and compared SP-induced histamine release with SD normotensive MCs.…”

Section: Discussionmentioning

confidence: 99%

“…Neuropeptides, including SP, are being increasingly recognized as important factors in the development of adverse cardiac remodelling and heart failure (D'Souza et al, 2007;Dehlin and Levick, 2014;Mak et al, 2011;Mak et al, 2015;Morrey et al, 2010;Ng et al, 2014;Robinson et al, 2009;Robinson et al, 2016;Weglicki et al, 1994;Widiapradja et al, 2017), and MCs are also important in the development of numerous cardiac pathologies (Batlle et al, 2007;Brower et al, 2002;Brower and Janicki, 2005;Frangogiannis et al, 1998;Levick et al, 2009;Marone et al, 1995;McLarty et al, 2011;Olivetti et al, 1989;Stewart et al, 2003). Therefore, it is important to better understand neuropeptide interactions with cardiac MCs.…”

Section: Introductionmentioning

confidence: 99%

Substance P-mediated cardiac mast cell activation: An in vitro study

2019

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The neuropeptide substance P can induce degranulation of cardiac mast cells at high concentrations. Herein, we seek to further understand substance P activation of cardiac mast cells in the context of other neuropeptides as well as modulation by non-neuropeptides. This is important given the increasingly recognized role of both cardiac mast cells and substance P in adverse cardiac remodeling. To address this, we isolated cardiac mast cells and compared their response to substance P as well as other members from the tachykinin family of peptides, including neurokinin A and hemokinin-1. We also tested the ability of other factors to manipulate the cardiac mast cell response to substance P. We found that while neurokinin A did not induce cardiac mast cell degranulation, both substance P and hemokinin-1 induced a concentrationdependent release of histamine; the maximal response to hemokinin-1 was greater than to substance P. Neurokinin-1 receptor blockade prevented substance P-induced histamine release, while only partially attenuating hemokinin-1-induced histamine release. The antioxidant Nacetylcysteine attenuated histamine release in response to hemokinin-1 and had no effect on substance P-induced histamine release. Selective PPAR-γ agonists attenuated histamine release in response to substance P. These data indicate that substance P activates cardiac mast cells via the neurokinin-1 receptor, and that the activation response is different to other tachykinins. That the response to substance P is receptor mediated and can be modulated by activation of other receptors (PPAR-γ), argues that substance P activation of cardiac mast cells has potential biological significance.

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“…As to cluster 8, we noted that a few genes were uniquely expressed with varied functions. These include Apoe, Tgfbi ; Wif1 , which modulates cardiomyocyte differentiation 46 necessary for cardiac remodeling in myocardial infarction and also promotes DCM 47 ; Clu , myocardial injury marker 48 ; and Npy, which has a role in cardiac remodeling and heart failure 49 . These data indicated that clusters 5, 6, and 8 were mainly involved in the cardiac remodeling process in myocarditis.…”

Section: Resultsmentioning

confidence: 99%

Dissecting the Cellular Landscape and Transcriptome Network in Viral Myocarditis by Single-Cell RNA Sequencing

Lasrado

Borcherding

Arumugam

et al. 2021

Preprint

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Myocarditis induced with Coxsackievirus B3 (CVB3) is commonly employed to study viral pathogenesis in mice. Although infectious virus is cleared after the acute phase, affected animals chronically develop the features of dilated cardiomyopathy, which may involve the mediation of immune and non-immune cells. To dissect this complexity, we performed single-cell RNA sequencing on heart cells obtained from healthy and myocarditic mice, leading us to note that myocarditic mice had significantly higher proportions of myeloid cells, CD4 and CD8 T cells, and fibroblasts, whereas NK cells, ILCs and B cells were low. While the transcriptome profiles of myeloid cells revealed detection of monocytes and macrophages of M2 phenotype with pathways important in immune metabolism and inflammation, T cells consisted of Th17 cells, CTLs, and Treg cells with transcriptome signatures critical for cytotoxic functions. Although fibroblasts detected in myocarditic mice were phenotypically heterogeneous, their transcriptomes played roles in fibrosis and regulation of inflammation and immune responses. Additionally, analysis of intercellular communication networks revealed unique interactions and signaling pathways in the cardiac cellulome, whereas myeloid cells and T cells in myocarditic mice revealed uniquely upregulated transcription factors modulating cardiac remodeling functions. Taken together, our data suggest that M2 cells, T cells, and fibroblasts may cooperatively or independently participate in the pathogenesis of viral myocarditis.

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The role of neuropeptides in adverse myocardial remodeling and heart failure

Cited by 19 publications

References 215 publications

The Role of Neuropeptide Y in Cardiovascular Health and Disease

The Role of Neuropeptide Y in Cardiovascular Health and Disease

Substance P-mediated cardiac mast cell activation: An in vitro study

Dissecting the Cellular Landscape and Transcriptome Network in Viral Myocarditis by Single-Cell RNA Sequencing

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