Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway
Braz. arch. biol. technol
;
60: e17160333, 2017. graf
Artículo
en Inglés
| LILACS
| ID: biblio-951471
ABSTRACT
ABSTRACT Odanacatib (ODN) is a selective inhibitor of cathepsin K. The cysteine protease cathepsin K has been implicated in cardiac hypertrophy. Resistine is an adipokine which is identified to promote cardiac hypertrophy. Here, we hypothesize that ODN mitigates resistin-induced myocyte hypertrophy. Cell surface area and protein synthesis were measured after treatment with resistin and ODN in H9c2 cells. The expression of cardiomyocyte hypertrophy marker BNP and β-MHC was detected by RT-qPCR. The expression and phosphorylation of AMPK and LKB1 were analyzed with Western blot. Resistin could significantly increase cardiomyocyte cell surface area, protein synthesis, and embryonic gene BNP and β-MHC expression, inhibit phosphorylation of AMPK and LKB1. ODN could significantly reverse the effects of resistin. Collectively, our data suggest that ODN can inhibit cardiomyocyte hypertrophy induced by resistin and the underlying mechanism may be involved in LKB1/AMPK pathway.
Texto completo:
Disponible
Índice:
LILACS (Américas)
Idioma:
Inglés
Revista:
Braz. arch. biol. technol
Asunto de la revista:
Biologia
Año:
2017
Tipo del documento:
Artículo
/
Documento de proyecto
País de afiliación:
China
Institución/País de afiliación:
Huaihe Hospital of Henan University/CN
/
Shanxi Medical University/CN
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