ABSTRACT
Aim: To explore whether RIP140 and TNF-a regulate energy metabolism in cardiomyocytes. Methods: H9c2 cardiomyocytes were infected with Ad-RIP140, simultaneously with or without TNF-α treatment. The mRNA levels of PPAR-α, PPAR-β/δ, and PDK4 were measured. H9c2 was exposed to adenovirus expressing RIP140-specific or nonspecific control. Expression of p65 in the nucleus and IκB-α: in cytoplasm were measured by Western blotting, and mRNA levels of IL-1β, IL-2 and TNF-α were measured by real-time PCR. H9c2 was treated with or without TNF-α. The mRNA and protein levels of RIP140 were measured. Results: Overexpression of RIP140 led to a decrease in mRNA levels of PPAR-α, PPAR-β/δ, PDK4, while TNF-α aggravated down-regulation of key metabolic genes by superabundant RIP140. A marked increase of p65-NF-κB in nuclear, a significant decrease of IκB-α in cytoplasm and a notable increase in mRNA levels of TNF-α, IL-β and IL-2 in H9c2 cell line were observed following overexpression of RIP140. The mRNA and protein levels of RIP140 were up-regulated by TNF-α treatment. Conclusions: RIP140 and TNF-a may collaborate in mediating proinflammatory processes and metabolic dysregulation in cardiomyocytes.