The adipocyte fatty acid–binding protein aP2 is required in allergic airway inflammation
J. Clin. Invest. Bennett O.V. Shum, et al. 116:2183 doi:10.1172/JCI24767 [
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Figure 3
Differential expression and regulation of
aP2
expression by PPARγ activation in HBEs and adipocytes.
(
A) HBEs and 3T3-L1 preadipocytes were treated with rosiglitazone (Ros.) or vehicle control and
aP2 mRNA expression assessed. Data represent mean of 3 HBE and two 3T3-L1 experiments. (
B)
CD36 message levels were determined in HBEs after rosiglitazone treatment. Data represent mean of 2 experiments. (
C) Relative abundance of
aP2 message from 100 ng RNA was compared among human adipose tissue, HBEs, HBEs plus IL-4, THP-1 monocytes, and THP-1 monocytes plus PMA. (
D) Transient transfection of BEAS-2B cells with WT STAT6, constitutively active STAT6 mutant (STAT6VT), or empty vector plasmids for 72 hours.
aP2 expression was monitored by real-time PCR. Data represent mean ± SEM of 3 experiments. *
P < 0.05 compared with vector control. (
E) Transient transfection of BEAS-2B cells with STAT6 dominant negative (STAT6DN) or empty vector plasmids. Twenty-four hours after transfection, cells were treated with IL-4 for 18 hours, and
aP2 transcript was quantified. Data represent mean ± SEM of 4 experiments. (
F) Time course of
aP2 expression in WT AECs after 3 or 18 hours treatment with IL-4 and TNF-α. Data represent the mean results from 2 independent cultures. (
G) STAT6-deficient AECs were cultured in vitro and treated with IL-4 for 18 hours, and
aP2 mRNA expression was assessed. Data represent the mean results of 2 independent cultures.
