The Adipokine Chemerin Induces Apoptosis in Cardiomyocytes

Autors de IIS La Fe

• Jose Manuel Varela Aguilar

  Autor

• Manuel Portoles Sanz

  Autor

• 

  Esther Roselló Lletí

  Autor

• Jose Miguel Rivera Otero

  Autor

• Carlos Gonzalez Juanatey

  Autor

• José Francisco Dolz Lago

  Autor

Autors aliens a IIS La Fe

• Rodríguez-Penas D
• Feijóo-Bandín S
• García-Rúa V
• Mosquera-Leal A
• Durán D
• Diéguez C
• Gualillo O

Grups d'Investigació

• Grupo de Investigación Clínica y Traslacional en Cardiología

  

  Investigador Principal

  Esther Roselló Lletí

Abstract

Background: The adipokine chemerin has been associated with cardiovascular disease. We investigated the effects of chemerin on viability and intracellular signalling in murine cardiomyocytes, and the effects of insulin and TNF-alpha on cardiomyocyte chemerin production. Methods: Hoechst dye vital staining and cell cycle analysis were used to analyse the viability of murine cardiac cells in culture. Western blot was used to explore the phosphorylation of AKT and caspase-9 activity in neonatal rat cardiomyocytes and HL-1 cells. Finally, RT-qPCR, ELISA and western blot were performed to examine chemerin and CMKLR1 expression after insulin and TNF-alpha treatment in cardiac cells. Results: Chemerin treatment increased apoptosis, reduced phosphorylation of AKT at Thr308 and increased caspase-9 activity in murine cardiomyocytes. Insulin treatment lowered chemerin and CMKLR1 mRNA and protein levels, and the amount of chemerin in the cell media, while TNF-alpha treatment increased chemerin mRNA and protein levels but decreased expression of the CMKLR1 gene. Conclusion: Chemerin induces apoptosis, reduces AKT phosphorylation and increases the cleavage of caspase-9 in murine cardiomyocytes. The expression of chemerin is regulated by important metabolic (insulin) and inflammatory (TNF-alpha) mediators at cardiac level. Our results suggest that chemerin could play a role in the physiopathology of cardiac diseases. Introduction Copyright (C) 2015 S. Karger AG, Basel

Keywords

• Cardiomyocyte; HL-1; Apoptosis; TNF-alpha; Insulin resistance; AKT; Chemerin