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Virology. 2017 Feb;502:133-143. doi: 10.1016/j.virol.2016.12.022. Epub 2016 Dec 30.

NF-κB activation is cell type-specific in the heart.

Author information

1
Department of Molecular Biomedical Sciences, North Carolina State University, Raleigh, NC, USA; Comparative Medicine Institute, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA.
2
Department of Molecular Biomedical Sciences, North Carolina State University, Raleigh, NC, USA; Comparative Medicine Institute, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA. Electronic address: barbara_sherry@ncsu.edu.

Abstract

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.

KEYWORDS:

Cardiac fibroblast; Cardiac myocyte; Cardiomyocyte; Golgi; Heart; Myocarditis; NF-κB; Reovirus

PMID:
28043025
PMCID:
PMC5276732
DOI:
10.1016/j.virol.2016.12.022
[Indexed for MEDLINE]
Free PMC Article

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