Abstract
Abstract RGS2 protein is well known as a negative regulator of GPCR signaling. In our previous research, we understood that RGS2 mRNA expression is decreased by TLR4, and thereby foam cell formation is induced. The present study proved how the decreased RGS2 regulates specific gene, Nox-1, expression. While TLR2 stimulation increased Nox-1 expression and decreased RGS2 expression in wild type mice macrophages, such phenomena did not occur with TLR2 KO mice macrophages. Nox-1 expression increase by TLR2 was intensified by RGS2 siRNA, and was inhibited by RGS2 overexpression. TLR2 stimulation caused phosphorylation of tyrosine 705 and serine 727 residues, and STAT3 siRNA inhibited Nox-1 expression by TLR2. RGS2 directly associated with STAT3 acting as a negative regulator by inhibiting Nox-1 expression by TLR2. PKC-eta and PLD2 also participated in Nox-1 regulation by controlling RGS2 expression. Overall, these results suggest that TLR2 stimulation decreases RGS2 expression mediating PKC-eta and PLD2, and thereby will increase Nox-1 expression by releasing the transcription ability of STAT3 restrained by RGS2.
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