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Cells
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Altered Cellular Communication in Cardiac Diseases
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Altered Cellular Communication in Cardiac Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (15 December 2022) | Viewed by 18582

Special Issue Editors

Dr. Thomas Wieland

E-Mail Website
Guest Editor
Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany
Interests: altered signal transduction in cardiovascular disease; GPCRs; Heterotrimeric G proteins; monomeric GTPases
Dr. Friederike Cuello

E-Mail Website
Guest Editor
Institute of Experimental Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Interests: altered signal transduction in cardiovascular disease; protein kinase regulation of cardiovascular function; redox control of physiological cell functions
Dr. Susanne Lutz

E-Mail Website
Guest Editor
Department of Pharmacology, University of Göttingen, Göttingen, Germany
Interests: mechanisms involved in cardiac fibrosis; G protein signaling; mechanotransduction; tissue engineering

Special Issue Information

Dear Colleagues,

Cardiac diseases are still one of the most prominent causes of morbidity and mortality worldwide. In heart failure, cardiac remodeling is first an adaptive, later a maladaptive, compensatory mechanism that finally causes ventricular dysfunction. Several cell types, as well as the extracellular matrix of the heart, contribute to these processes with their basic functions and their intercellular communications, both under normal and pathological conditions. In recent years, the number of novel factors and mediators contributing to the cross-talk of cardiomyocytes with endothelial cells, cardiac fibroblasts, myeloid cells and the extracellular matrix has constantly increased. Thus, compiling the knowledge of mechanisms of cellular communication by the established or the more recently discovered agents will create a platform for new perspectives in the prevention and treatment of heart failure and other cardiac diseases.

The aim of this Special Issue is to assemble original data and reviews depicting a plethora of cellular communication and signaling that characterizes heart function in health and disease. We hope that contributions from expert laboratories will result in a compendium supporting researchers with an established interest in heart function, but also help young researchers to get immediate access to this fascinating area of cellular interplay and organ function.

Dr. Thomas Wieland
Dr. Friederike Cuello
Dr. Susanne Lutz
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cell communication
  • cardiac remodeling
  • cardiomyocytes
  • cardiac fibroblasts
  • endothelial cells
  • vascular smooth muscle cells
  • myeloid cells
  • extracellular matrix

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Published Papers (6 papers)

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Research

Jump to: Review

13 pages, 1264 KiB  
Article
The Muscarinic Acetylcholine M2 Receptor-Induced Nitration of p190A by eNOS Increases RhoA Activity in Cardiac Myocytes
by Magdolna K. Levay, Lena Throm, Nabil Bahrami and Thomas Wieland
Cells 2023, 12(20), 2432; https://doi.org/10.3390/cells12202432 - 11 Oct 2023
Viewed by 1137
Abstract
p190RhoGAP, which exists in two paralogs, p190RhoGAP-A (p190A) and p190RhoGAP-B (p190B), is a GTPase activating protein (GAP) contributing to the regulation of the cellular activity of RhoGTPases. Recent data showed that M2 muscarinic acetylcholine receptor (M2R) stimulation in neonatal rat [...] Read more.
p190RhoGAP, which exists in two paralogs, p190RhoGAP-A (p190A) and p190RhoGAP-B (p190B), is a GTPase activating protein (GAP) contributing to the regulation of the cellular activity of RhoGTPases. Recent data showed that M2 muscarinic acetylcholine receptor (M2R) stimulation in neonatal rat cardiac myocytes (NRCM) induces the binding of p190RhoGAP to the long isoform of the regulator of G protein signaling 3 (RGS3L). This complex formation alters the substrate preference of p190RhoGAP from RhoA to Rac1. By analyzing carbachol-stimulated GAP activity, we show herein that p190A, but not p190B, alters its substrate preference in NRCM. Based on data that the RhoGAP activity of p190A in endothelial cells is diminished upon nitration by endothelial nitric oxide synthase (eNOS)-derived peroxynitrite, we studied whether carbachol-induced NO/peroxynitrite formation contributes to the carbachol-induced RhoA activation in NRCM. Interestingly, the carbachol-induced RhoA activation in NRCM was suppressed by the eNOS-preferring inhibitor L-NIO as well as the non-selective NOS inhibitor L-NAME. Using L-NIO, we firstly verified the carbachol-induced NO production concurrent with eNOS activation and, secondly, the carbachol-induced nitration of p190A in NRCM. By co-immunoprecipitation, the carbachol-induced complex formation of eNOS, p190A, RGS3L and caveolin-3 was detected. We thus conclude that the NO production by M2R-induced eNOS activation in caveolae in NRCM is required for the nitration of p190A, leading to the binding to RGS3L and the change in substrate preference from RhoA to Rac1. In line with this interpretation, the disruption of caveolae in NRCM by methyl-β-cyclodextrin suppressed carbachol-induced RhoA activation in NRCM to a similar extent as the inhibition of NO production. Full article
(This article belongs to the Special Issue Altered Cellular Communication in Cardiac Diseases)
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20 pages, 6626 KiB  
Article
C1q and Tumor Necrosis Factor Related Protein 9 Protects from Diabetic Cardiomyopathy by Alleviating Cardiac Insulin Resistance and Inflammation
by Ricarda Haustein, Felix A. Trogisch, Merve Keles, Susanne Hille, Manuela Fuhrmann, Nina Weinzierl, Shruthi Hemanna, James Thackeray, Yanliang Dou, Carolin Zwadlo, Natali Froese, Julio Cordero, Frank Bengel, Oliver J. Müller, Johann Bauersachs, Gergana Dobreva and Joerg Heineke
Cells 2023, 12(3), 443; https://doi.org/10.3390/cells12030443 - 29 Jan 2023
Cited by 1 | Viewed by 2966
Abstract
(1) Background: Diabetic cardiomyopathy is a major health problem worldwide. CTRP9, a secreted glycoprotein, is mainly expressed in cardiac endothelial cells and becomes downregulated in mouse models of diabetes mellitus; (2) Methods: In this study, we investigated the impact of CTRP9 on early [...] Read more.
(1) Background: Diabetic cardiomyopathy is a major health problem worldwide. CTRP9, a secreted glycoprotein, is mainly expressed in cardiac endothelial cells and becomes downregulated in mouse models of diabetes mellitus; (2) Methods: In this study, we investigated the impact of CTRP9 on early stages of diabetic cardiomyopathy induced by 12 weeks of high-fat diet; (3) Results: While the lack of CTRP9 in knock-out mice aggravated insulin resistance and triggered diastolic left ventricular dysfunction, AAV9-mediated cardiac CTRP9 overexpression ameliorated cardiomyopathy under these conditions. At this early disease state upon high-fat diet, no fibrosis, no oxidative damage and no lipid deposition were identified in the myocardium of any of the experimental groups. Mechanistically, we found that CTRP9 is required for insulin-dependent signaling, cardiac glucose uptake in vivo and oxidative energy production in cardiomyocytes. Extensive RNA sequencing from myocardial tissue of CTRP9-overexpressing and knock-out as well as respective control mice revealed that CTRP9 acts as an anti-inflammatory mediator in the myocardium. Hence, CTRP9 knock-out exerted more, while CTRP9-overexpressing mice showed less leukocytes accumulation in the heart during high-fat diet; (4) Conclusions: In summary, endothelial-derived CTRP9 plays a prominent paracrine role to protect against diabetic cardiomyopathy and might constitute a therapeutic target. Full article
(This article belongs to the Special Issue Altered Cellular Communication in Cardiac Diseases)
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24 pages, 5603 KiB  
Article
Cysteine-Rich LIM-Only Protein 4 (CRP4) Promotes Atherogenesis in the ApoE−/− Mouse Model
by Natalie Längst, Julia Adler, Anna Kuret, Andreas Peter, Peter Ruth, Karsten Boldt and Robert Lukowski
Cells 2022, 11(8), 1364; https://doi.org/10.3390/cells11081364 - 17 Apr 2022
Cited by 4 | Viewed by 3172
Abstract
Vascular smooth muscle cells (VSMCs) can switch from their contractile state to a synthetic phenotype resulting in high migratory and proliferative capacity and driving atherosclerotic lesion formation. The cysteine-rich LIM-only protein 4 (CRP4) reportedly modulates VSM-like transcriptional signatures, which are perturbed in VSMCs [...] Read more.
Vascular smooth muscle cells (VSMCs) can switch from their contractile state to a synthetic phenotype resulting in high migratory and proliferative capacity and driving atherosclerotic lesion formation. The cysteine-rich LIM-only protein 4 (CRP4) reportedly modulates VSM-like transcriptional signatures, which are perturbed in VSMCs undergoing phenotypic switching. Thus, we hypothesized that CRP4 contributes to adverse VSMC behaviours and thereby to atherogenesis in vivo. The atherogenic properties of CRP4 were investigated in plaque-prone apolipoprotein E (ApoE) and CRP4 double-knockout (dKO) as well as ApoE-deficient CRP4 wildtype mice. dKO mice exhibited lower plaque numbers and lesion areas as well as a reduced content of α-smooth muscle actin positive cells in the lesion area, while lesion-associated cell proliferation was elevated in vessels lacking CRP4. Reduced plaque volumes in dKO correlated with significantly less intra-plaque oxidized low-density lipoprotein (oxLDL), presumably due to upregulation of the antioxidant factor peroxiredoxin-4 (PRDX4). This study identifies CRP4 as a novel pro-atherogenic factor that facilitates plaque oxLDL deposition and identifies the invasion of atherosclerotic lesions by VSMCs as important determinants of plaque vulnerability. Thus, targeting of VSMC CRP4 should be considered in plaque-stabilizing pharmacological strategies. Full article
(This article belongs to the Special Issue Altered Cellular Communication in Cardiac Diseases)
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Review

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19 pages, 1831 KiB  
Review
Cellular Mechanisms Mediating Exercise-Induced Protection against Cardiotoxic Anthracycline Cancer Therapy
by Sanela Dozic, Erin J. Howden, James R. Bell, Kimberley M. Mellor, Lea M. D. Delbridge and Kate L. Weeks
Cells 2023, 12(9), 1312; https://doi.org/10.3390/cells12091312 - 4 May 2023
Cited by 12 | Viewed by 3626
Abstract
Anthracyclines such as doxorubicin are widely used chemotherapy drugs. A common side effect of anthracycline therapy is cardiotoxicity, which can compromise heart function and lead to dilated cardiomyopathy and heart failure. Dexrazoxane and heart failure medications (i.e., beta blockers and drugs targeting the [...] Read more.
Anthracyclines such as doxorubicin are widely used chemotherapy drugs. A common side effect of anthracycline therapy is cardiotoxicity, which can compromise heart function and lead to dilated cardiomyopathy and heart failure. Dexrazoxane and heart failure medications (i.e., beta blockers and drugs targeting the renin–angiotensin system) are prescribed for the primary prevention of cancer therapy-related cardiotoxicity and for the management of cardiac dysfunction and symptoms if they arise during chemotherapy. However, there is a clear need for new therapies to combat the cardiotoxic effects of cancer drugs. Exercise is a cardioprotective stimulus that has recently been shown to improve heart function and prevent functional disability in breast cancer patients undergoing anthracycline chemotherapy. Evidence from preclinical studies supports the use of exercise training to prevent or attenuate the damaging effects of anthracyclines on the cardiovascular system. In this review, we summarise findings from experimental models which provide insight into cellular mechanisms by which exercise may protect the heart from anthracycline-mediated damage, and identify knowledge gaps that require further investigation. Improved understanding of the mechanisms by which exercise protects the heart from anthracyclines may lead to the development of novel therapies to treat cancer therapy-related cardiotoxicity. Full article
(This article belongs to the Special Issue Altered Cellular Communication in Cardiac Diseases)
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13 pages, 3286 KiB  
Review
Actin-Binding Proteins in Cardiac Hypertrophy
by Congbin Pan, Siqi Wang, Chao Liu and Zhanhong Ren
Cells 2022, 11(22), 3566; https://doi.org/10.3390/cells11223566 - 11 Nov 2022
Cited by 2 | Viewed by 4348
Abstract
The heart reacts to a large number of pathological stimuli through cardiac hypertrophy, which finally can lead to heart failure. However, the molecular mechanisms of cardiac hypertrophy remain elusive. Actin participates in the formation of highly differentiated myofibrils under the regulation of actin-binding [...] Read more.
The heart reacts to a large number of pathological stimuli through cardiac hypertrophy, which finally can lead to heart failure. However, the molecular mechanisms of cardiac hypertrophy remain elusive. Actin participates in the formation of highly differentiated myofibrils under the regulation of actin-binding proteins (ABPs), which provides a structural basis for the contractile function and morphological change in cardiomyocytes. Previous studies have shown that the functional abnormality of ABPs can contribute to cardiac hypertrophy. Here, we review the function of various actin-binding proteins associated with the development of cardiac hypertrophy, which provides more references for the prevention and treatment of cardiomyopathy. Full article
(This article belongs to the Special Issue Altered Cellular Communication in Cardiac Diseases)
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14 pages, 1119 KiB  
Review
Redox Regulation of Soluble Epoxide Hydrolase—Implications for Cardiovascular Health and Disease
by Rebecca Charles and Philip Eaton
Cells 2022, 11(12), 1932; https://doi.org/10.3390/cells11121932 - 15 Jun 2022
Cited by 5 | Viewed by 2368
Abstract
Cell responses to changes in their redox state are significantly mediated by reversible oxido-reductive post-translational modifications of proteins, potentially altering their activities or interactions. These modifications are important for the homeostatic responses of cells to environmental changes that alter their redox state. Such [...] Read more.
Cell responses to changes in their redox state are significantly mediated by reversible oxido-reductive post-translational modifications of proteins, potentially altering their activities or interactions. These modifications are important for the homeostatic responses of cells to environmental changes that alter their redox state. Such redox regulatory mechanisms not only operate to maintain health, but can become dysregulated and contribute to pathophysiology. In this review, we focus on the redox control of soluble epoxide hydrolase (sEH), which is widely expressed, including in blood vessels and cardiomyocytes. We review the different types of oxidative modifications that regulate sEH and how they may alter cardiovascular physiology and affect disease progression during stress. Full article
(This article belongs to the Special Issue Altered Cellular Communication in Cardiac Diseases)
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