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. 2009 Oct 22;44(2):135–142. doi: 10.1677/JME-09-0090

Figure 1.

Figure 1

Rosiglitazone activation of PPARγ down-regulates FR in macrophages. (A) Northern blot analyses of RNA expression in TPA-differentiated THP-1 macrophages. THP-1 cells were differentiated with TPA (40 ng/ml) for 48 h before being treated with rosiglitazone (BRL, 1 μM) or GW501516 (GW, 0·1 μM) for the indicated amount of time. RNA was isolated and analyzed by northern blot using gene-specific probes. (B) Quantification of the northern blot analyses of FR and LXR in 1A with PhosphorImager. The expression of FR and LXR was normalized by the expression of GADPH. (C) Northern blot analyses of RNA expression in undifferentiated THP-1 monocytes. THP-1 cells were treated with rosiglitazone (BRL, 1 μM) or GW501516 (GW, 0·1 μM) for the indicated amount of time in the absence of TPA. RNA was isolated and analyzed by northern blot using gene-specific probes. (D and E) RNA expression analysis of FR in bone marrow-derived macrophages (BMDMs) (D) and thioglycollate-elicited peritoneal macrophages (E). Primary mouse macrophages were treated with rosiglitazone (BRL, 1 μM), GW501516 (GW, 0·1 μM), or LG100268 (LG268, 0·1 μM) for 24 h. RNA was isolated and analyzed by RT-QPCR. FR expression was normalized by the expression of the ribosomal protein gene L19. All experiments were repeated at least three times, and representative results are shown. *Indicates P<0·05; **indicates P<0·01.