The Adipokine Chemerin Induces Apoptosis in Cardiomyocytes

Autor: Diego Rodríguez-Penas, Sandra Feijóo-Bandín, Vanessa García-Rúa, Ana Mosquera-Leal, Darío Durán, Alfonso Varela, Manuel Portolés, Esther Roselló-Lletí, Miguel Rivera, Carlos Diéguez, Oreste Gualillo, José Ramón González-Juanatey, Francisca Lago
Jazyk: angličtina
Rok vydání: 2015
Předmět:
Zdroj: Cellular Physiology and Biochemistry, Vol 37, Iss 1, Pp 176-192 (2015)
Druh dokumentu: article
ISSN: 1015-8987
1421-9778
DOI: 10.1159/000430343
Popis: 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-α 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-α 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-α 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-α) mediators at cardiac level. Our results suggest that chemerin could play a role in the physiopathology of cardiac diseases.
Databáze: Directory of Open Access Journals
Externí odkaz: