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NF-κB activation is cell type-specific in the heart
Efraín E Rivera-Serrano1, Barbara Sherry1
1Department 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.
Insights
Viral infections can cause myocarditis, leading to heart failure. This study reveals nuclear factor-kappa B (NF-κB) activation differs between cardiac cells, impacting inflammatory responses and heart damage.
Area of Science:
- Cardiology
- Molecular Biology
- Immunology
Background:
- Viral myocarditis is a significant cause of heart failure.
- Cardiac inflammation is crucial for viral clearance but can cause damage.
- Nuclear factor-kappa B (NF-κB) controls inflammatory cytokine expression, but its cell-type-specific activation in the heart is unclear.
Purpose of the Study:
- To compare basal and induced NF-κB activation in cardiac myocytes and cardiac fibroblasts.
- To investigate cell type-specific inflammatory signaling in the heart during viral infection.
Main Methods:
- Primary cultures of cardiac myocytes and cardiac fibroblasts were used.
- NF-κB activation was assessed in response to viral infection.
- Subcellular localization of NF-κB was analyzed in different cardiac cell types.
Main Results:
- Viral infection strongly activated NF-κB in cardiac fibroblasts.
- Cardiac myocytes showed limited NF-κB activation.
- Cardiac myocyte subpopulations exhibited distinct NF-κB subcellular localization, with the cis-Golgi identified as a specific compartment.
Conclusions:
- NF-κB signaling in the heart is cell type-specific.
- These differences may represent a mechanism to balance protective and damaging inflammatory responses in the heart.
- Understanding cell-specific NF-κB activation is crucial for managing viral myocarditis and cardiac inflammation.
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.
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