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BOR - Papers in Press, published online ahead of print September 26, 2007.
Biol Reprod 2007, 10.1095/biolreprod.107.063479
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Submitted June 18, 2007
Returned for revision July 16, 2007
Accepted September 17, 2007

Pregnancy


Role of Protein Kinase C Isozymes in the Regulation of alpha1-Adrenergic Receptor-Mediated Contractions in Ovine Uterine Arteries

Hongying Zhang and Lubo Zhang *

* To whom correspondence should be addressed. E-mail: lzhang{at}llu.edu.

Abstract
Previously, we demonstrated that activation of protein kinase C (PRKC) enhanced alpha1 adrenergic receptor-induced contractions in nonpregnant ovine uterine arteries (NPUA), but inhibited the contractions in pregnant ovine uterine arteries (PUA). The present study tested the hypothesis that differential regulation of PRKC isozyme activities contributes to the different effects of phorbol 12, 13-dibutyrate (PDBu) on alpha1 adrenergic receptor-mediated contractions between the pregnant and nonpregnant ovine uterine arteries. Phenylephrine-induced contractions of ovine NPUA and PUA were determined in the absence or presence of the PRKC activator PDBu, and/or conventional and novel PRKC isozymes inhibitor GF109203X, PRKC isozyme-selective inhibitory peptides for conventional PRKC, PRKCB1, PRKCB2 and PRKCE, respectively. GF109203X produced a concentration-dependent inhibition of phenylephrine-induced contractions in both NPUA and PUA, and reversed the PDBu-mediated potentiation and inhibition of phenylephrine-induced contractions in NPUA and PUA, respectively. In addition, PRKCB1, PRKCB2 and PRKCE inhibitory peptides blocked the PDBu-mediated responses in both NPUA and PUA. Western blot analysis showed that PDBu induced a membrane translocation of PRKCA, PRKCB1, PRKCB2 and PRKCE in PUA, and PRKCB1, PRKCB2 and PRKCE in NPUA. The results disprove the hypothesis that the dichotomy of PRKC mechanisms in the regulation of alpha1 adrenergic receptor-induced contraction in nonpregnant and pregnant uterine arteries is caused by the activation of different PRKC isozymes, and suggest down-stream mechanisms of differential sub-cellular distributions for the distinct functional effects of PRKC isozymes in the adaptation of uterine arteries to pregnancy.

Key words: Pregnancy • GF109203X • Protein kinase C • phenylephrine • phorbol 12, 13-dibutyrate




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