| Full text | |
| Author(s): |
Cruz Junho, V, C.
;
Trentin-Sonoda, M.
[1, 2]
;
Alvim, J. M.
[1, 3]
;
Gaisler-Silva, F.
[1]
;
Carneiro-Ramos, M. S.
[1]
Total Authors: 5
|
| Affiliation: | [1] Cruz Junho, C., V, Univ Fed ABC, Ctr Ciencias Nat & Humanas, Santo Andre, SP - Brazil
[2] Univ Ottawa, Fac Med, Cellular & Mol Med, Ottawa, ON - Canada
[3] Univ Sao Paulo, Hosp Clin, Fac Med, Lab Genet & Cardiol Mol, Inst Coracao, Sao Paulo, SP - Brazil
Total Affiliations: 3
|
| Document type: | Journal article |
| Source: | Brazilian Journal of Medical and Biological Research; v. 52, n. 7 2019. |
| Web of Science Citations: | 1 |
| 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 (CaMKII delta B) 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 CaMKII delta B 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, CaMKII delta B silencing attenuated nuclear factor-kappa B expression. These findings supported the hypothesis that CaMKII delta B 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 CaMKII delta B. 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, CaMKII delta B 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 |