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. Author manuscript; available in PMC: 2014 May 3.
Published in final edited form as: Sci Transl Med. 2013 Nov 27;5(213):213ra164. doi: 10.1126/scitranslmed.3007148

Fig. 6. Vpr increases lipolysis in adipocytes.

Fig. 6

(A) Timeline indicates chronology of lentivirus infection, differentiation medium addition, and doxycycline addition (late). (B and C) Lipolysis (FFA and glycerol release), basal and after stimulation with vehicle or CL316243 (β3-adrenoceptor agonist), in 3T3-L1 cells 72 hours after doxycycline. Vpr increased FFA release (P = 0.05). (D) Quantification of PPARγ- or GR-associated sequences of AdipoQ, Ap2, and Hsl after ChIP of PPARγ or GR after rosiglitazone or dexamethasone treatment 24 hours after doxycycline. Data are representative of three experiments. Binding site levels of AdipoQ (P = 0.001) and Ap2 (P = 0.01) were lower, and that of Hsl (P = 0.004) was higher, in Vpr compared to control (rtTA) condition. Off-target DNA sequences ~2 kb upstream of the PPARγ/GR-binding sites were amplified as negative controls (NC). 3T3-L1, no lentivirus; rtTA, infected with control virus; Vpr, infected with WT-Vpr virus; Vpr-R80A, infected with Vpr-R80A mutant virus. Values are means ± SE. *P < 0.05, **P < 0.01, ***P < 0.001.