Some patients with Group A Streptococcal toxic shock syndrome (StrepTSS) develop a unique form of cardiomyopathy characterized by global hypokinesia and reduced cardiac index. Here we investigated the immune responses of cardiomyocytes to Group A Streptococcus both in vivo and in vitro. Our data demonstrate that cardiomyocyte-derived cytokines are produced following both direct GAS stimulation and after exposure to GAS-activated inflammatory cells. These locally produced, cardiomyocyte-derived cytokines may mediate cardiac contractile dysfunction observed in patients with StrepTSS-associated cardiomyopathy and may hold the key to our ability to attenuate this severe complication.
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http://dx.doi.org/10.1016/j.cyto.2011.02.009 | DOI Listing |
J Extracell Vesicles
November 2024
Department of Experimental Cardiology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Extracellular vesicles (EVs) have emerged as important mediators of intercellular communication in the heart under homeostatic and pathological conditions, such as myocardial infarction (MI). However, the basic mechanisms driving cardiomyocyte-derived EV (CM-EV) production following stress are poorly understood. In this study, we generated human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) that express NanoLuc-tetraspanin reporters.
View Article and Find Full Text PDFJ Mol Cell Cardiol
March 2024
Department of Human Health and Nutritional Sciences, University of Guelph, 50 Stone Road East, Guelph, ON N1G 2W1, Canada; IMPART investigator Team, Canada. Electronic address:
The role of erythropoietin (EPO) has extended beyond hematopoiesis to include cytoprotection, inotropy, and neurogenesis. Extra-renal EPO has been reported for multiple tissue/cell types, but the physiological relevance remains unknown. Although the EPO receptor is expressed by multiple cardiac cell types and human recombinant EPO increases contractility and confers cytoprotection against injury, whether the heart produces physiologically meaningful amounts of EPO in vivo is unclear.
View Article and Find Full Text PDFSci China Life Sci
May 2023
Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing, 100191, China.
Rapid over-activation of β-adrenergic receptors (β-AR) following acute stress initiates cardiac inflammation and injury by activating interleukin-18 (IL-18), however, the process of inflammation cascades has not been fully illustrated. The present study aimed to determine the mechanisms of cardiac inflammatory amplification following acute sympathetic activation. With bioinformatics analysis, galectin-3 was identified as a potential key downstream effector of β-AR and IL-18 activation.
View Article and Find Full Text PDFPeerJ
January 2023
Department of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Ferroptosis is a mode of cell death that occurs in myocardial infarction (MI). Signals emanating from apoptotic cells are able to induce macrophage polarization through exosome-loading cargos, which plays a vital role in the process of disease. However, whether ferroptotic cardiomyocytes derived exosome (MI-Exo) during MI act on macrophage polarization and its mechanism remain unclear.
View Article and Find Full Text PDFJ Mol Cell Cardiol
September 2020
Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hannover, Germany,; REBIRTH Excellence Cluster, Hannover Medical School, Hannover, Germany. Electronic address:
Myocardial ischemia induces a multifaceted remodeling process in the heart. Novel therapeutic entry points to counteract maladaptive signalling include the modulation of non-coding RNA molecules such as long non-coding RNA (lncRNA). We here questioned if the lncRNA candidate H19 exhibits regulatory potential in the setting of myocardial infarction.
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