Abstract
7 Dominant negative mutations which inactivate the peroxisome proliferator-activated receptor gamma (PPARγ) nuclear receptor in man are associated with severe insulin resistance, diabetes and hypertension (Barroso I et al. Nature, 1999;402:880-883). Using RNase protection assay, Western blot analysis and immunostaining of cultured primary rat mesangial cells, we identified the presence of PPARγ message and protein. Electrophoretic mobility of a labeled PPARγ response element (PPRE) was retarded in the presence of mesangial cell nuclear extract, suggesting that PPARγ is functional in these cells. Addition of unlabelled PPRE efficiently competed away the PPARγ-PPRE protein complex, confirming specificity of binding of the PPARγ to the PPRE. PPARγ ligands, rosiglitazone (10 μM) and troglitazone (10 μM), both completely inhibited platelet derived growth factor (PDGF)-induced DNA synthesis measured as bromodeoxyuridine (BrdU) incorporation (p
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