Mechanisms of arginine-vasopressin-induced Ca2+ oscillations in beta-cells (HIT-T15): a role for oscillating protein kinase C

Endocrinology
Michael SchaeferChristof Schöfl

Abstract

We examined the role of protein kinase C (PKC) for the generation of arginine-vasopressin (AVP)-linked Ca2+ oscillations in beta-cells (HIT-T15). Activation of PKC by phorbol-12,13-dibutyrate (PDBu) reduced the frequency and finally abolished AVP-induced Ca2+ oscillations. The PKC inhibitors Gö 6976, Ro-32-0432, or chelerythrine converted Ca2+ oscillations to a plateau-like rise in cytosolic free Ca2+, and PKC down-regulation reduced the percentage of cells exhibiting AVP-induced Ca2+ oscillations. Several mechanisms were identified by which PKC could exert feedback on the AVP-linked Ca2+ oscillator. PDBu, but not the PKC inhibitors, inhibited AVP-stimulated inositol 1,4,5-trisphosphate production and mobilization of internal Ca2+. Ca2+ influx through voltage-sensitive Ca2+ channels was attenuated by PDBu and PKC inhibitors, indicating complex PKC-dependent regulation of voltage-sensitive Ca2+ channels involving stimulatory as well as inhibitory components. Furthermore, AVP caused oscillatory translocation of yellow fluorescent protein (YFP)-tagged PKCalpha and PKCbetaIota to the plasma membrane, which paralleled the Ca2+ oscillations in single cells. Repetitive translocation of YFP-PKCalpha and -PKCbetaIota could also be elici...Continue Reading

Citations

Mar 2, 2006·Molecular and Cellular Biology·Alejandra CollazosDominique Joubert
Nov 28, 2007·The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society·Miho OyasuNaoaki Saito
Apr 25, 2008·The Journal of Endocrinology·Anne-Marie O'CarrollStephen J Lolait
Aug 19, 2008·Frontiers in Neuroendocrinology·Zvi Naor
Jan 11, 2008·Physical Biology·Minchul Kang, Hans G Othmer

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