Project description:Cardiac pathological hypertrophy is associated with a significantly increased risk of coronary heart disease and has been observed in diabetic patients treated with rosiglitazone, whereas most published studies do not suggest a similar increase in risk of cardiovascular events in pioglitazone-treated diabetic subjects. This study sought to understand the pathophysiological mechanisms underlying the disparate cardiovascular effects of rosiglitazone and pioglitazone and yield knowledge as to the causative nature of rosiglitazone-associated cardiac hypertrophy.
Project description:Pioglitazone treatment of CD4+FoxP3- T cells transduced with Pparg and Foxp3 up-regulated a set of genes whose products have been implicated in lipid metabolism pathways. To verify the specificity of this treatment, we performed microarray analysis on Foxp3+Pparg1-transduced CD4+FoxP3- T cells after treatment with other PPARg agonists such as Rosiglitazone (TZD) and GW1929 (non-TZD).
Project description:Cardiac pathological hypertrophy is associated with a significantly increased risk of coronary heart disease and has been observed in diabetic patients treated with rosiglitazone, whereas most published studies do not suggest a similar increase in risk of cardiovascular events in pioglitazone-treated diabetic subjects. This study sought to understand the pathophysiological mechanisms underlying the disparate cardiovascular effects of rosiglitazone and pioglitazone and yield knowledge as to the causative nature of rosiglitazone-associated cardiac hypertrophy. Total RNA obtained from mouse Apex from LDLr-/- mice treated with High Fat diet (HF) diet as control (n=6) or HF+Pio (n=5) or HF+Rosi (n=5).