Effects of a proteasome inhibitor on cardiomyocytes in a pressure-overload hypertrophy rat model: An animal study
- Authors
- Kim, I.-S.; Jo, W.-M.
- Issue Date
- 2017
- Publisher
- Korean Society for Thoracic and Cardiovascular Surgery
- Keywords
- Androgen; Cardiomyopathy; Hypertrophic; MG132; NF-kappa B; Proteasome inhibitors; Receptors; Ubiquitins
- Citation
- Korean Journal of Thoracic and Cardiovascular Surgery, v.50, no.3, pp.144 - 152
- Indexed
- SCOPUS
KCI
- Journal Title
- Korean Journal of Thoracic and Cardiovascular Surgery
- Volume
- 50
- Number
- 3
- Start Page
- 144
- End Page
- 152
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/86114
- DOI
- 10.5090/kjtcs.2017.50.3.144
- ISSN
- 2233-601X
- Abstract
- Background: The ubiquitin-proteasome system (UPS) is an important pathway of proteolysis in pathologic hypertrophic cardiomyocytes. We hypothesize that MG132, a proteasome inhibitor, might prevent hypertrophic cardiomyopathy (CMP) by blocking the UPS. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and androgen receptor (AR) have been reported to be mediators of CMP and heart failure. This study drew upon pathophysiologic studies and the analysis of NF-κB and AR to assess the cardioprotective effects of MG132 in a left ventricular hypertrophy (LVH) rat model. Methods: We constructed a transverse aortic constriction (TAC)-induced LVH rat model with 3 groups: sham (TAC-sham, n=10), control (TAC-cont, n=10), and MG132 administration (TAC-MG132, n=10). MG-132 (0.1 mg/kg) was injected for 4 weeks in the TAC-MG132 group. Pathophysiologic evaluations were performed and the expression of AR and NF-κB was measured in the left ventricle. Results: Fibrosis was prevalent in the pathologic examination of the TAC-cont model, and it was reduced in the TAC-MG132 group, although not significantly. Less expression of AR, but not NF-κB, was found in the TAC-MG132 group than in the TAC-cont group (p<0.05). Conclusion: MG-132 was found to suppress AR in the TAC-CMP model by blocking the UPS, which reduced fibrosis. However, NF-κB expression levels were not related to UPS function. © The Korean Society for Thoracic and Cardiovascular Surgery. 2017.
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