Adipokine-induced activation responses in vascular endothelial cells: An inflammatory trigger in adipose microenvironment (CAM4P.160)

Abstract

Abstract Obesity is a global epidemic and leads to premature death due to its association with metabolic diseases. Evidence suggests that a low-grade, chronic inflammation of adipose tissue contributes to metabolic disorder of visceral adipose tissue. Adipose tissue-derived hormones, also called as adipokines, regulate variety of homeostatic functions, including metabolism and inflammation. We examined the function of adipokines: visfatin, vaspin and leptin, and tested the hypothesis that adipokines regulate immunoinfiltration of adipose tissue by inducing activation of endothelium in the adipose microenvironment. A large scale microarray was performed for the identification of soluble chemokines produced by adipokine-treated endothelial cells, and a decrease in the levels of chemokine ligand-17 was observed (n=5). Further, ELISA analysis confirmed significant upregulation for pro-inflammatory chemokines: Monocyte chemoattractant protein-1 (MCP-1) and granulocyte monocyte-colony stimulating factor (p<0.05, n=5). RNA was isolated from the adipokine-treated endothelial cells and real-time PCR analysis confirmed significant upregulation of pro-inflammatory genes interleukin-6 and MCP-1 in response to visfatin treatment (p<0.05, n=5). The surface expression of adhesion markers was measured by flow cytometry, and vascular cell adhesion protein-1 was found upregulated in response to visfatin. Overall, our results suggest that the studied adipokines are functional link for ECs and leukocyte crosstalk in the context of the adipose tissue.