2016 journal article

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

VIROLOGY, 502, 133–143.

By: E. Rivera-Serrano n & B. Sherry n

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
TL;DR: 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. (via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
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.