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Inflammatory activation of human cardiac fibroblasts leads to altered calcium signaling, decreased connexin 43 expression and increased glutamate secretion

Journal article
Authors Eva Skiöldebrand
Annika Lundqvist
Ulrika Björklund
Mikael Sandstedt
Anders Lindahl
Elisabeth Hansson
Lillemor Mattsson Hultén
Published in Heliyon
Volume 3
Issue 10
ISSN 2405-8440
Publication year 2017
Published at Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
Institute of Medicine, Department of Molecular and Clinical Medicine
Language en
Links doi.org/10.1016/j.heliyon.2017.e004...
Keywords Biochemistry, Biological sciences, Cardiology, Cell biology, Health sciences, Immunology, Internal medicine, Medicine
Subject categories Cardiac and Cardiovascular Systems

Abstract

Cardiac fibroblasts, which are abundant in heart tissue, are involved not only in extracellular matrix homeostasis and repair, but also in cardiac remodeling after a myocardial infarction that, in turn, can lead to loss of cardiac function and heart failure. Ca2+ signaling is functionally important in many cell types, but the roles of fibroblast signaling and inflammation in the pathogenesis of heart disease are unclear. Here, we tested the hypothesis that inflammatory activation affects cardiac fibroblasts, both in terms of Ca2+ signaling and their capacity for intercellular communication through the gap junction channel protein connexin 43 (Cx43). We examined Ca2+ responses induced by known modulators of cardiac function such as glutamate, ATP and 5-hydroxytryptamine (5-HT) in human cardiac fibroblasts, under normal and inflammatory conditions. We showed that activation of human cardiac fibroblasts by lipopolysaccharide (LPS) for 24 h altered Ca2+ signaling, increased TLR4 and decreased Cx43 expression. In the fibroblasts, LPS treatment increased glutamate-evoked and decreased 5-HT-evoked Ca2+ signals. LPS activation also induced increased secretion of glutamate and proinflammatory cytokines from these cells. In summary, we propose that inflammatory stimuli can affect intracellular Ca2+ release, Cx43 expression, glutamate release and cytokine secretion in human cardiac fibroblasts. Inflammatory conditions may, therefore, impair intercellular network communication between fibroblasts and cardiomyocytes potentially contributing to cardiac dysfunction. © 2017 The Authors

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