p300, a transcriptional co-activator with histone acetyl transferase (HAT) 
activity, plays an essential role in the pathogenesis of cardiomyocyte 
hypertrophy in response to multiple pro-hypertrophic stimuli including 
hyperglycemia. However, the precise mechanisms by which p300 expression is 
regulated remain unclear. The purpose of this study was to investigate the role 
of miR-150, a potential p300-targeting microRNA (miRNA), in the 
post-transcriptional control of p300 expression and cardiomyocyte hypertrophy 
induced by high glucose. We observed that the expression of miR-150 was 
significantly reduced, whereas the expression of p300 was strongly elevated, 
concomitant with cardiomyocyte hypertrophy, in the hearts of diabetic rats 
compared with normal controls. Similar alterations were observed in neonatal rat 
cardiomyocytes that had been exposed to high levels of glucose. miR-150 mimics 
inhibited p300 3'-UTR luciferase reporter activity, as well as endogenous p300 
expression. In addition, miR-150 mimics prevented glucose-induced cardiomyocyte 
hypertrophy. Co-transfection with a p300 expression vector and miR-150 mimics 
reversed the protective effect of miR-150 on cardiomyocyte hypertrophy. We 
further showed that the high glucose-mediated activation of PKCβ(2) in turn 
mediated the down-regulation of miR-150 expression. These data demonstrated a 
novel upstream role for miR-150 in p300-mediated cardiomyocyte hypertrophy and 
revealed a previously uncharacterized miRNAs and HATs cross-talk mechanism for 
the hypertrophic phenotype induced by high glucose.