ArticleBiology of reproduction2008
Role of protein kinase C isozymes in the regulation of alpha1-adrenergic receptor-mediated contractions in ovine uterine arteries.
Article in Biology of reproduction, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Perivascular Adipose Tissue and Uterine Artery Adaptations to Pregnancy.Microcirculation (New York, N.Y. : 1994) · 2024Review
- CaInternational journal of molecular sciences · 2023Review
- PKC regulates alpha(1)-adrenoceptor-mediated contractions and baseline Ca(2+) sensitivity in the uterine arteries of nonpregnant and pregnant sheep acclimatized to high altitude hypoxia.High altitude medicine & biology · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Previously, we demonstrated that activation of protein kinase C (PRKC) enhanced alpha(1)-adrenergic receptor-induced contractions in nonpregnant ovine uterine arteries but inhibited the contractions in pregnant ovine uterine arteries. 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 alpha(1)-adrenergic receptor-mediated contractions between the pregnant and nonpregnant ovine uterine arteries. Phenylephrine-induced contractions of ovine nonpregnant and pregnant uterine arteries were determined in the absence or presence of the PRKC activator PDBu and/or in combination with conventional and novel PRKC isozyme inhibitor GF109203X, PRKC isozyme-selective inhibitory peptides for conventional PRKC, PRKCB1, PRKCB2, and PRKCE. GF109203X produced a concentration-dependent inhibition of phenylephrine-induced contractions in both nonpregnant and pregnant uterine arteries, and it reversed the PDBu-mediated potentiation and inhibition of phenylephrine-induced contractions in nonpregnant and pregnant uterine artieries, respectively. In addition, PRKCB1, PRKCB2, and PRKCE inhibitory peptides blocked the PDBu-mediated responses in both nonpregnant and pregnant uterine arteries. Western blot analysis showed that PDBu induced a membrane translocation of PRKCA, PRKCB1, PRKCB2, and PRKCE in pregnant uterine arteries, and PRKCB1, PRKCB2, and PRKCE in nonpregnant uterine arteries. The results disprove the hypothesis that the dichotomy of PRKC mechanisms in the regulation of alpha(1)-adrenergic receptor-induced contractions in nonpregnant and pregnant uterine arteries is caused by the activation of different PRKC isozymes, and suggest downstream mechanisms of differential subcellular distributions for the distinct functional effects of PRKC isozymes in the adaptation of uterine arteries to pregnancy.
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Registered trials
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