Abstract P142: Inflammation Upregulates Adipocyte Expression of (Pro)renin Receptor

Abstract

Obesity represents a state of chronic inflammation in adipose tissue and this inflammation contributes to obesity related comorbidities. Our laboratory has previously demonstrated that the (Pro)renin receptor (PRR) promotes the production of proinflammatory factors via the ERK-MAP kinase pathway. We have also shown that in the setting of renal inflammation, NF-κB increases renal expression of PRR by binding to the PRR promoter. In this study we hypothesized that inflammation increases expression of PRR in adipose tissue. We monitored changes in expression of PRR mRNA by RT-PCR and protein by western blot in 3T3-L1 adipocytes treated with 100ng/ml LPS or normal culture medium (control) for 24 hours. To confirm that LPS treatment effectively induced an inflammatory response in 3T3-L1 adipocytes, we monitored production of the inflammatory cytokine, IL-6, in culture media by luminex assay. Compared to control, LPS significantly increased IL-6 production (48.8 pg/mL in controls vs. 1877 pg/mL in LPS treated cells, p<0.05). Similarly, compared to control, LPS treatment increased adipocyte expression of PRR mRNA and protein by 120% and 62%, (p<0.05) respectively (figure 1). We conclude that inflammation increases adipocyte expression of PRR, suggesting that PRR may play a role in obesity related adipose tissue inflammation and obesity associated pathology.