Premium
Angiotensin II upregulates PPARgamma gene and transcriptional activity during 3T3‐L1 adipocyte differentiation via the AT1 receptor subtype
Author(s) -
Bharadwaj Kalyani G,
Bruemmer Dennis C,
Cassis Lisa Ann
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.lb107
Subject(s) - losartan , angiotensin ii , endocrinology , medicine , adipocyte , angiotensin ii receptor type 1 , receptor , peroxisome proliferator activated receptor , chemistry , biology , adipose tissue
Previous reports have demonstrated an increase in expression of components of the renin‐angiotensin system during the course of adipocyte differentiation, suggesting a proadipogenic role of angiotensin II (AngII). The purpose of this study was to examine the effect of AngII on PPARγ as a marker of adipocyte differentiation in 3T3‐L1 adipocytes. 3T3‐L1 preadipocytes were induced to differentiate two days post‐confluence. AngII (1uM) was incubated with cells 1 day post confluence and was maintained in the media through day 6. AngII significantly increased PPARγ mRNA expression on day 6. To determine the receptor subtype mediating the effect of AngII, cells were treated with losartan (AT1 receptor antagonist) or PD123319 (AT2 receptor antagonist) in the absence or presence of AngII. Losartan did not alter basal PPARγ mRNA expression, but antagonized the induction of PPARγ mRNA expression by AngII. In contrast, PD123319 increased basal PPARγ mRNA expression and this increase was maintained in the presence of AngII. To determine if AngII increased PPARγ activity, cells were transiently transfected with a PPRE construct fused to luciferase reporter gene on day 4 of differentiation followed by incubation with AngII for 48 hours. AngII resulted in a modest but significant increase in PPARγ transcriptional activity. These results demonstrate that AngII increases PPARγ mRNA expression and activity in differentiating adipocytes through effects at the AT1 receptor.