In situ determination of [Ca2+]i threshold for translocation of the alpha-protein kinase C isoform

DOI Web Site 被引用文献1件
  • R. A. Khalil
    Cardiovascular Division, Charles A. Dana Research Institute,Harvard-Thorndike Laboratory, Beth Israel Hospital, Boston,Massachusetts.
  • C. Lajoie
    Cardiovascular Division, Charles A. Dana Research Institute,Harvard-Thorndike Laboratory, Beth Israel Hospital, Boston,Massachusetts.
  • K. G. Morgan
    Cardiovascular Division, Charles A. Dana Research Institute,Harvard-Thorndike Laboratory, Beth Israel Hospital, Boston,Massachusetts.

書誌事項

公開日
1994-06-01
DOI
  • 10.1152/ajpcell.1994.266.6.c1544
公開者
American Physiological Society

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説明

<jats:p> Because of inherent difficulties in maintaining physiological conditions in biochemical assays, the intracellular free Ca2+ concentration ([Ca2+]i) required for activation of protein kinase C (PKC) in intact cells remains unclear. In the present study, [Ca2+]i was measured in freshly isolated vascular smooth muscle cells loaded with fura 2 while, in parallel, the distribution of the Ca(2+)-dependent alpha-PKC isoform was monitored using digital imaging microscopy. The [Ca2+]i alpha-PKC translocation threshold was determined by changing extracellular free Ca2+ concentration in steps while monitoring [Ca2+]i. In the absence of agonists, increasing [Ca2+]i caused < 25% of maximal translocation. In the presence of phenylephrine, maximum translocation occurred at [Ca2+]i > or = 198 nM. Phenylephrine augmented translocation of alpha-PKC primarily by increasing the slope of the [Ca2+]i-PKC translocation relationship. These results indicate that the [Ca2+]i threshold of alpha-PKC translocation in situ is less than that reported in most in vitro assays and are consistent with an effect of agonist-induced generation of other second messengers that cause cooperative interactions leading to translocation. </jats:p>

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