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Overexpression of CTRP3 protects against sepsis-induced myocardial dysfunction in mice.
- Source :
-
Molecular & Cellular Endocrinology . Nov2018, Vol. 476, p27-36. 10p. - Publication Year :
- 2018
-
Abstract
- Abstract C1q/tumor necrosis factor-related protein-3 (CTRP3) shows striking homologies of genomic structure to the adiponectin. In this study, we aimed to investigate the protective role of CTRP3 against sepsis-induced cardiomyopathy. Here, we overexpressed CTRP3 in myocardium by direct intramyocardial injection and constructed a model of lipopolysaccharide (LPS)-induced sepsis in mice. Our results demonstrated that cardiac-specific overexpression of CTRP3 remarkably attenuated myocardial dysfunction and increased the phosphorylation level of AMPKα during LPS-induced sepsis. The anti-inflammatory effects of CTRP3, as determined by decreased mRNA levels of TNF-α, IL-6 and a lower protein expression of phosphorylated NF-κB p65 and IκBα, was detected in mice following LPS treatment. Additionally, CTRP3 suppressed cardiac apoptosis induced by LPS in mice as indicated by terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining and western blot for Cleaved-caspase3, Bax and Bcl-2. In conclusion, CTRP3 could protect against sepsis-induced myocardial dysfunction in mice. The cardioprotective effects of CTRP3 might be mediated by activating AMPKα signaling pathway and blunting inflammatory response and apoptosis. Highlights • LPS stimulation elevates the cardiac CTRP3 expression in mice. • Overexpression of CTRP3 alleviates the sepsis-induced myocardial dysfunction and activates AMPK signaling pathway. • Overexpression of CTRP3 attenuates the inflammatory response and apoptosis during LPS induced septic cardiomyopathy. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 03037207
- Volume :
- 476
- Database :
- Academic Search Index
- Journal :
- Molecular & Cellular Endocrinology
- Publication Type :
- Academic Journal
- Accession number :
- 131525501
- Full Text :
- https://doi.org/10.1016/j.mce.2018.04.006