ISSN:
1471-4159
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Abstract: In rat pinealocytes, cytoplasmic alkalization causes protein kinase C (PKC) translocation, but the isozyme involved is not known. In this study, we investigated the effect of cytoplasmic alkalization on membrane-associated PKCα, δ, ε, and ζ, four isozymes present in the rat pineal gland. Treatment with NH4Cl, which had no effect on PKCζ, caused a sustained increase in membrane-associated PKCα, δ, and ε that lasted for at least 60 min. The effect of NH4Cl on PKCα, δ, and ε was reduced by sodium propionate, an agent that counteracts the effect of NH4Cl on intracellular pH. Both sodium propionate and 5-(N,N-hexamethylene)amiloride (HMA), two treatments that abolished the effect of norepinephrine on cytoplasmic alkalization, also reduced norepinephrine-mediated increases in membrane-associated PKCα, δ, and ε. In contrast, these two treatments did not have an effect on the increase in membrane-associated PKC isozymes caused by 4β-phorbol 12-myristate 13-acetate (PMA), an active phorbol ester, even though HMA was effective in abolishing PMA-mediated increases in intracellular pH. These results, apart from demonstrating that cytoplasmic alkalization by itself can cause translocation of PKCα, δ, and ε in rat pinealocytes, also indicate that the norepinephrine-stimulated cytoplasmic alkalization plays an important role in transducing signals from the adrenergic receptor to selective PKC isozymes. However, PKC translocation stimulated directly by PMA does not appear to be sensitive to changes in intracellular pH.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1046/j.1471-4159.2000.0751845.x
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