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. 2003 Feb 26;100(5):2730–2735. doi: 10.1073/pnas.0538015100

Figure 5.

Figure 5

Enzymatically intact LPL induces PPARα target gene mRNA expression. (A Left) HepG2 cells were transfected (24 h, DMEM, 1% delipidated serum) with empty vector (PcDNA3), human WT LPL, or a catalytically inactive LPL (mutant LPL), and expression levels were confirmed with RT-PCR (data not shown). Northern analysis reveals that VLDL treatment (5 μg/ml, 3 h) induced ACO mRNA expression in LPL-treated cells, but not if they had been pretreated (15 min) with tetrahydrolipostatin (THL, 10 μM). HepG2 cells expressing the mutant LPL had no ACO induction after VLDL treatment. (Right) Similar Northern results are seen in HEK293 cells transfected and stimulated as before. (B) The concentration response of ACO mRNA expression to VLDL was tested in HepG2 cells incubated with LPL (200 units/ml, 1 h). (C) LPL/VLDL treatment induces ACO and LPL mRNA expression in human Mφ treated with LPL/VLDL as described in Fig. 5B. One representative result of three is shown. (D) In vivo analysis of skeletal muscle from WT LPL-overexpressing/PPARα+/+, and LPL-overexpressing/PPARα−/− mice reveals increased peroxisomal proliferation with LPL overexpression in the presence but not absence of PPARα. Peroxisomal expression from fasting mice (age 12 wk, n = 3) was analyzed by using PMP70 antibody.