| pubmed-article:12616990 | pubmed:abstractText | We have previously reported that prolonged exposure of porcine coronary arteries to adenosine agonists upregulates protein kinase C (PKC) through the activation of adenosine A1 receptor-coupled to pertussis toxin sensitive G-protein(s) [Am. J. Physiol. 264 (1993) H1465; Am. J. Physiol. 269 (1995) H1619]. The mechanism(s) by which A1 adenosine receptor upregulates PKC (isoforms) are not yet clearly understood. In the present study, we identified the alpha, beta 1, beta 2, gamma, epsilon, and zeta PKC isoforms that were upregulated by adenosine A1 receptor agonist as a possible mechanism(s) involved for this upregulation. Incubation of porcine coronary smooth muscle cells (PCSMC) with adenosine A1 receptor agonist (2s)-N6-[2-endo-norbornyl]adenosine (ENBA) caused an upregulation of PKC (isoforms), which were blocked by adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). Western blot analysis using specific antibodies to PKC isoforms indicated that all the isoforms tested (alpha, beta I, beta II, mu, gamma, delta, epsilon, and zeta) were present in the primary cultured smooth muscle cells from porcine coronary artery. Western blot studies indicated that PKC alpha, beta I, beta II, gamma, epsilon, and zeta isoforms were upregulated in a dose dependent manner by adenosine agonist (ENBA) and PKC delta and mu were not altered. | lld:pubmed |
