2017 journal article

NF-kappa B activation is cell type-specific in the heart

VIROLOGY, 502, 133–143.

co-author countries: United States of America 🇺🇸
author keywords: NF-kappa B; Myocarditis; Cardiac myocyte; Cardiac fibroblast; Cardiomyocyte; Golgi; Reovirus; Heart
MeSH headings : Animals; Cell Line; Cells, Cultured; Fibroblasts / metabolism; Fibroblasts / virology; Golgi Apparatus / metabolism; Golgi Apparatus / virology; Heart / virology; Humans; Mammalian orthoreovirus 3 / physiology; Mice; Mice, Inbred C57BL; Myocytes, Cardiac / metabolism; Myocytes, Cardiac / virology; NF-kappa B / genetics; NF-kappa B / metabolism; Organ Specificity; Reoviridae Infections / genetics; Reoviridae Infections / metabolism; Reoviridae Infections / virology; Signal Transduction
Source: Web Of Science
Added: August 6, 2018

Viral myocarditis is common and can progress to cardiac failure. Cardiac cell pro-inflammatory responses are critical for viral clearance, however sustained inflammatory responses contribute to cardiac damage. The transcription factor NF-κB regulates expression of many pro-inflammatory cytokines, but basal and induced activation of NF-κB in different cardiac cell types have not been compared. Here, we used primary cultures of cardiac myocytes and cardiac fibroblasts to identify cardiac cell type-specific events. We show that while viral infection readily stimulates activation of NF-κB in cardiac fibroblasts, cardiac myocytes are largely recalcitrant to activation of NF-κB. Moreover, we show that cardiac myocyte subpopulations differ in their NF-κB subcellular localization and identify the cis-Golgi as a cardiac myocyte-specific host compartment. Together, results indicate that NF-κB-dependent signaling in the heart is cardiac cell type-specific, likely reflecting mechanisms that have evolved to balance responses that can be either protective or damaging to the heart.