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. Author manuscript; available in PMC: 2008 Aug 15.
Published in final edited form as: Mol Cell Endocrinol. 2007 May 29;274(1-2):35–42. doi: 10.1016/j.mce.2007.05.013

Fig.1. LPS, but not fatty acid free LPS, inhibits expression of the dominant GHR (L2-GHR) transcript.

Fig.1

(A) RAW 264.7 cells, which express endogenous TLR4 and MD2, were co-transfected with L2-promoter-luciferase reporter (pGL3-L2-2.0 kb) and pRL-TK (internal control) plasmids. 24 h after transfection, cells were stimulated with either vehicle or the indicated concentration of LPS for 5-6 h and cells harvested and luciferase activity measured. Results are expressed as mean ± SEM; n = 3-4, p < 0.05 (Kruskal Wallis test) compared to the luciferase activity in the absence of LPS (vehicle). (B) BNL.CL2 cells, stably expressing the L2 promoter-luciferase construct were exposed to 1μg/ml of either LPS or fatty acid free LPS. 48 h later, the cells were harvested and the luciferase activity measured. Luciferase activity, normalized for protein content, is expressed relative to activity observed with exposure of the cells to vehicle (PBS) alone. Results are expressed as mean ±SEM; n=4. p < 0.01 (Mann-Whitney U test) compared to the luciferase activity in the absence of LPS (vehicle).