Ca2+/Calmodulin-dependent kinase II delta B is essential for cardiomyocyte hypertrophy and complement gene expression after LPS and HSP60 stimulation in vitro

Ca2+/Calmodulin-dependent kinase II delta B is essential for cardiomyocyte hypertrophy and complement gene expression after LPS and HSP60 stimulation in vitro

Inflammation plays an important role in the development of cardiovascular diseases (CVDs), suggesting that the immune system is a target of therapeutic interventions used for treating CVDs. This study evaluated mechanisms underlying inflammatory response and cardiomyocyte hypertrophy associated with...

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Published in:Brazilian journal of medical and biological research Vol. 52; no. 7; p. e8732
Main Authors: Cruz Junho, C V, Trentin-Sonoda, M, Alvim, J M, Gaisler-Silva, F, Carneiro-Ramos, M S
Format: Journal Article
Language:English
Published: Brazil Revista Brasileira de Pesquisas Medicas 01-01-2019
Associação Brasileira de Divulgação Científica
Subjects:
BIOLOGY
Calcium-binding protein
Calmodulin
CaMKII
Cardiomyocytes
Cardiovascular diseases
Complement
Complement activation
Complement component C3
Complement factor B
Gene expression
Heat shock proteins
Hsp60 protein
Hypertrophy
Immune system
Inflammation
Interleukin 6
Kinases
Lipopolysaccharides
MEDICINE, RESEARCH & EXPERIMENTAL
NF-κB protein
siRNA
Therapeutic applications
TLR 2/4
Toll-like receptors
Transcription
Cardiomyocytes
Inflammation
Complement
CaMKII
Hypertrophy
TLR 2/4
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Summary:Inflammation plays an important role in the development of cardiovascular diseases (CVDs), suggesting that the immune system is a target of therapeutic interventions used for treating CVDs. This study evaluated mechanisms underlying inflammatory response and cardiomyocyte hypertrophy associated with bacterial lipopolysaccharide (LPS)- or heat shock protein 60 (HSP60)-induced Toll-like receptor (TLR) stimulation and the effect of a small interfering RNA (siRNA) against Ca2+/calmodulin-dependent kinase II delta B (CaMKIIδB) on these outcomes. Our results showed that treatment with HSP60 or LPS (TLR agonists) induced cardiomyocyte hypertrophy and complement system C3 and factor B gene expression. In vitro silencing of CaMKIIδB prevented complement gene transcription and cardiomyocyte hypertrophy associated with TLR 2/4 activation but did not prevent the increase in interleukin-6 and tumor necrosis factor-alfa gene expression in primary cultured cardiomyocytes. Moreover, CaMKIIδB silencing attenuated nuclear factor-kappa B expression. These findings supported the hypothesis that CaMKIIδB acts as a link between inflammation and cardiac hypertrophy. Furthermore, the present study is the first to show that extracellular HSP60 activated complement gene expression through CaMKIIδB. Our results indicated that a stress stimulus induced by LPS or HSP60 treatment promoted cardiomyocyte hypertrophy and initiated an inflammatory response through the complement system. However, CaMKIIδB silencing prevented the cardiomyocyte hypertrophy independent of inflammatory response induced by LPS or HSP60 treatment.
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These authors contributed equally to this work.
ISSN:0100-879X
1414-431X
1414-431X
1678-4510
DOI:10.1590/1414-431X20198732