Thiazolidinediones up-regulate insulin-like growth factor-1 receptor via a peroxisome proliferator-activated receptor gamma-independent pathway.

ABSTRACT: There is increasing evidence that thiazolidinediones (TZDs), antidiabetic compounds that are synthetic ligands for the peroxisome proliferator-activated receptor γ (PPARγ), have cardiovascular effects through as yet poorly defined mechanisms. We tested the effect of two TZD class drugs, rosiglitazone and pioglitazone, on human aortic smooth muscle cell (SMC) expression of insulin-like growth factor-1 receptor (IGF-1R). Both TZDs dose dependently up-regulated IGF-1R protein levels (rosiglitazone, 10 μmol/liter, 67% increase, n = 4, p < 0.01; pioglitazone, 10 μmol/liter, 41% increase, n = 4, p < 0.01) and increased IGF-1R signaling activity (36% increase in Akt phosphorylation). However, the endogenous PPARγ ligand, 15-deoxy-Δ(12,14)-prostaglandin J(2), dose dependently reduced IGF-1R (10 μm

SUBMITTER: Higashi Y 

PROVIDER: S-EPMC2978564 | biostudies-literature | 2010 Nov

REPOSITORIES: biostudies-literature