Figure 6.

RBP4-induced inflammation, oxidative stress and hypertrophy are TLR4 and MyD88 dependent. Primary cardiomyocytes were isolated from Tlr4 and Myd88 knockout (Tlr4^−/− and Myd88^−/−) or control mice and then treated with recombinant mouse RBP4 or vehicle control for 48 hours. A, mRNA expression of Tnf-α, Il-6, Mcp-1, and Il-1β. B, Secretion of TNF-α, IL-6, MCP-1, and IL-1β in the supernatant of cultured cardiomyocytes. C, Intracellular ROS production. D–G, Hypertrophy was assessed by cell size (D), cell surface area measurement (E), protein to DNA ratio (F), and analysis of the mRNA expression for Anp, Bnp, and Myh7 by qRT-PCR (G) (n = 6 per group). *, P < .05 vs control-WT; #, P < .05 vs RBP4-WT. Bar, 20 μm. AU, arbitrary units.