Gender Difference in Protein Kinase C β-II mRNA Expression in Rat Aorta: Implication in Hyperglycemia Induced Vascular Dysfunction

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To date little is known of the interactions between hyperglycemia and sex hormones in the vasculature. We previously showed that there is a gender difference in the high glucose induced impairment of the endothelium dependent vasodilation (EDV) in rat aorta, possibly via activation of Protein kinase C (PKC) ?. The objectives of the present study were to investigate, 1) if there is a gender specific difference in the mRNA expression level of PKC ?I and PKC ?II isoforms in rat aorta, 2) if PKC activation by Phorbol-12-myristate-13-acetate (PMA) mimics the effect of high glucose in female rat aorta, and 3) if the effect of PKC on EDV is blocked by selective inhibition of PKC ?. The mRNA expression of PKC ? isoforms were measured by semi-quantitative Reverse Transcriptase ? Polymerase Chain Reaction. Furthermore, dilator responses to acetylcholine (10-8 to 10-5M) were obtained before and after 3 hours treatment with PMA (0.5 ?M), in phenylephrine pre-contracted female rat aorta. The same experiment was generated in the presence and absence of a PKC ? inhibitor (1?M). We showed that 1) PKC ? II mRNA is expressed significantly higher in female rat aorta than its male counterpart, 2) activation of PKC by PMA impairs EDV in female rat aorta, and 3) inhibition of PKC ? prevents the PMA-induced impairment of EDV. These results suggest that impairment of EDV by acute exposure to high glucose in female rat aorta is possibly due to the high level of PKC ? II expression (Supported by NHLBI).