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A redistribution of actin and myosin IIA accompanies Ca(2+)-dependent insulin secretion


The study addressed the functional link between remodelling of the actomyosin cytoskeleton in pancreatic beta-cells and the regulation of insulin secretion. Confocal microscopy revealed that myosin heavy chain (MHC) IIA co-localized very well with filamentous (F)-actin in RINm5F cells but MHCIIB did not. Subcellular localization of MHCIIB was not altered by stimulation with 30 mM KCl (which evokes Ca(2+)-dependent insulin secretion). In contrast MHCIIA redistributed in a manner similar to F-actin, especially towards the apical surface, but also away from peripheral regions towards cell contact points on the basal surface. Finally, Ca(2+)-dependent insulin secretion was inhibited by stabilization of actin filaments with jasplakinolide. The results support a role for the MHCIIA/actin cytoskeleton in regulating insulin secretion.

Type Journal
ISBN 0014-5793 (Print)
Authors Wilson, J. R.;Ludowyke, R. I.;Biden, T. J. :
Publisher Name FEBS LETT
Published Date 2001-01-01 00:00:00
Published Volume 492
Published Issue 1-2
Published Pages 101-6
Status Published In-print