Adenovirus-mediated silencing of synaptotagmin 9 inhibits Ca2+-dependent insulin secretion in islets

FEBS Lett. 2005 Sep 26;579(23):5241-6. doi: 10.1016/j.febslet.2005.08.047.

Abstract

Synaptotagmins (Syts) are involved in Ca(2+)-dependent insulin release. However, which Syt isoform is functional in primary beta-cells remains unknown. We demonstrate by electron microscopy of pancreatic islets, the association of Syt 9 with insulin granules. Silencing of Syt 9 by RNA interference adenovirus in islet cells had no effect on the expression of Syt 5, Syt 7 and Syt 3 isoforms. The latter was localized at the plasma membrane of pancreatic polypeptide cells. Insulin release in response to glucose or tolbutamide was strongly inhibited in Syt 9 deficient islets, whereas exocytosis potentiated by raising cAMP levels, was unaltered. Thus, Syt 9 may act as Ca(2+) sensor for beta-cell secretion.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviridae / genetics
  • Adenoviridae / metabolism*
  • Animals
  • Calcium / metabolism*
  • Calcium-Binding Proteins / genetics
  • Calcium-Binding Proteins / metabolism*
  • Cell Line
  • Insulin / metabolism*
  • Islets of Langerhans / metabolism*
  • Islets of Langerhans / ultrastructure
  • Membrane Glycoproteins / metabolism
  • Mice
  • Nerve Tissue Proteins / metabolism
  • Protein Isoforms / metabolism
  • RNA Interference*
  • Rats
  • Synaptotagmins

Substances

  • Calcium-Binding Proteins
  • Insulin
  • Membrane Glycoproteins
  • Nerve Tissue Proteins
  • Protein Isoforms
  • Syt9 protein, rat
  • Synaptotagmins
  • Calcium