Abstract
Short-term Treatment of RAW264.7 Macrophages with Adiponectin Increases Tumor Necrosis Factor-α (TNF-α) Expression via ERK1/2 Activation and Egr-1 Expression
Highlights
Adiponectin (a 30-kDa peptide known as adipocyte complement-related protein; Acrp30)2 is an adipokine secreted by adipose tissue [1, 2]
We demonstrate that globular adiponectin initially increased TNF-␣ expression in RAW264.7 macrophages; this TNF-␣ contributed to increased expression of interleukin-10, which in turn was required for the development of tolerance to subsequent LPS exposure. gAcrp-mediated increases in TNF-␣ mRNA accumulation were associated with increased TNF-␣ promoter activity. gAcrp increased the DNA binding activity of both Egr-1 and NFB; mutation of either the Egr-1 or NFB binding sites in the TNF-␣ promoter decreased gAcrp-stimulated promoter activity
One recent report demonstrates that short-term treatment of macrophages with adiponectin first increases the expression of inflammatory cytokines, such as TNF-␣ and IL-6 [15]; continued exposure to adiponectin promotes the development of tolerance to subsequent pro-inflammatory signals, such as the toll-like receptor 4 ligand LPS or the toll-like receptor 3 ligand poly(I1⁄7C) [15]
Summary
Adiponectin (a 30-kDa peptide known as adipocyte complement-related protein; Acrp30)2 is an adipokine secreted by adipose tissue [1, 2]. Adiponectin Rapidly Activates ERK1/2 and Egr-1 anti-inflammatory mediators, such as IL-10 [16]; it is not yet known whether IL-10 is essential for the inhibitory effects of adiponectin on LPS-stimulated signaling in macrophages. We report a similar effect of an 18-h treatment with adiponectin on LPS-stimulated TNF-␣ protein secretion in RAW 264.7 macrophages (Fig. 1A).
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