Figure 9.SirT1 is necessary for mIGF-1-dependent upregulation of anti-oxidant and hypertrophic genes adiponectin, UCP1 and MT-2.(A)
Neonatal primary cardiomyocytes from wild type or mIGF-1 Tg mice were
treated with sirtinol (100 μM)
or EX-527 (1 μM), or treated
with 20 ng/ml IGF-1 for 24 h. (B) HL-1 cardiomyocytes were
transfected with the indicated plasmids, or treated with 20 ng/ml IGF-1 for
24 h. Untransfected cells were used as control (CTL). (A, B)
The expression levels of adiponectin, UCP-1 and MT-2 mRNAs were examined by
Real Time-PCR. (C) Neonatal primary cardiomyocytes from wild type or
mIGF-1 Tg mice, and HL-1 cardiomyocytes, were transfected with 1 μg of
plasmids carrying Firefly luciferase under the control of promoters of
adiponectin (Adipo-Luc), UCP1 (UCP1-Luc) and MT-2 (MT-2-Luc) genes,
respectively, together with 1 μg of Renilla Luciferase plasmid. Neonatal
primary cardiomyocytes were also treated with different inhibitors or IGF-1
as described in (A). Dual luciferase assays were performed in
duplicate for each condition. (A-C) Results are means ± SE of 3 independent experiments
(*,**,***p versus untreated
cardiomyocytes).
