| Full text | |
| Author(s): |
C.V. Cruz Junho
[1]
;
M. Trentin-Sonoda
;
J.M. Alvim
;
F. Gaisler-Silva
[4]
;
M.S. Carneiro-Ramos
[5]
Total Authors: 5
|
| Affiliation: | [1] Universidade Federal do ABC. Centro de Ciências Naturais e Humanas - Brasil
[4] Universidade Federal do ABC. Centro de Ciências Naturais e Humanas - Brasil
[5] Universidade Federal do ABC. Centro de Ciências Naturais e Humanas - Brasil
Total Affiliations: 5
|
| Document type: | Journal article |
| Source: | Brazilian Journal of Medical and Biological Research; v. 52, n. 7 2019-07-15. |
| Abstract | |
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. (AU) | |
| FAPESP's process: | 16/11865-0 - Participation of complement system in the cardiomyocyte hypertrophy induced by activation of toll-like receptor type 4 in vitro: the role of CaMKIId |
| Grantee: | Carolina Victória da Cruz Junho |
| Support Opportunities: | Scholarships in Brazil - Scientific Initiation |
| FAPESP's process: | 15/19107-5 - TLR4 and complement system : possible key mechanism in renal ischemia/reperfusion induced cardiac hypertrophy |
| Grantee: | Marcela Sorelli Carneiro Ramos |
| Support Opportunities: | Regular Research Grants |
| FAPESP's process: | 15/01792-3 - Contribution of complement system in renal ischemia/reperfusion induced cardiac hypertrophy: role of toll like receptor 4 |
| Grantee: | Carolina Victória da Cruz Junho |
| Support Opportunities: | Scholarships in Brazil - Scientific Initiation |
| FAPESP's process: | 14/16908-4 - The role of Toll-like receptors 2 and 4 in the development of cardiomyocyte hypertrophy in vitro: participation of NF-kB signaling |
| Grantee: | Juliana Morais Alvim |
| Support Opportunities: | Scholarships in Brazil - Scientific Initiation |