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. Author manuscript; available in PMC: 2015 Jun 30.
Published in final edited form as: J Immunol. 2012 Oct 26;189(11):5411–5420. doi: 10.4049/jimmunol.1201487

Figure 4. Genetic Deletion of ePPARγ Upregulates in vivo LPS Signaling.

Figure 4

ePPARγ+/+ and ePPARγ−/− mice were treated with LPS (10 mg/kg, i.p.). Twelve h later lung tissue protein extracts were prepared and the levels of LPS signaling proteins analyzed. Lungs of ePPARγ−/− mice exhibited higher levels of (A) the LPS receptor TLR4 and its downstream signaling molecules MyD88, IRAK-4, and TRAF6; B) the phosphorylated (activated) forms of intermediate signaling molecules further downstream (Akt, ERK, p38, JNK, IKKα/β); and (C) the transcription factors NF-κB (p65) and Nrf2. Blots were simultaneously incubated with lamin B1 or β-actin antibody where indicated. Smaller blot represents PBS treated ePPARγ+/+ mice (left), ePPARγ−/− mice (right). In larger blot left four lanes represent LPS treated ePPARγ+/+ mice, right four lanes represent LPS treated ePPARγ−/− mice. In separate experiments we also determined DNA-binding activities of transcription factors in lung extracts. ePPARγ KO abolished the LPS-induced component of (D) PPARγ activity, while (E) enhancing the LPS-induced decrease in Nrf2 activity and (F) markedly elevating LPS-induced NF-κB activity. Blots are representative of 3 independent experiments with each lane representing a single mouse lung, and activity data of 2 independent experiments (n = 6–8 mice per group). *** P < 0.001.