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

Iezzi, M; Eliasson, Lena LU ; Fukuda, M and Wollheim, C B (2005) In FEBS Letters 579(23). p.5241-5246
Abstract
Synaptotagmins (Syts) are involved in Ca2+-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 Ca2+ sensor for beta-cell secretion.
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
insulin exocytosis, pancreatic islets, electron, RNA, microscopy, interference, beta-cell
in
FEBS Letters
volume
579
issue
23
pages
5241 - 5246
publisher
Wiley-Blackwell
external identifiers
  • pmid:16165130
  • wos:000232194300024
  • scopus:24944458103
ISSN
1873-3468
DOI
10.1016/j.febslet.2005.08.047
language
English
LU publication?
yes
id
186553df-d08f-402a-a699-0ec381315ef9 (old id 223129)
date added to LUP
2007-08-03 10:28:24
date last changed
2017-01-29 04:06:09
@article{186553df-d08f-402a-a699-0ec381315ef9,
  abstract     = {Synaptotagmins (Syts) are involved in Ca2+-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 Ca2+ sensor for beta-cell secretion.},
  author       = {Iezzi, M and Eliasson, Lena and Fukuda, M and Wollheim, C B},
  issn         = {1873-3468},
  keyword      = {insulin exocytosis,pancreatic islets,electron,RNA,microscopy,interference,beta-cell},
  language     = {eng},
  number       = {23},
  pages        = {5241--5246},
  publisher    = {Wiley-Blackwell},
  series       = {FEBS Letters},
  title        = {Adenovirus-mediated silencing of Synaptotagmin 9 inhibits Ca2+-dependent insulin secretion in islets},
  url          = {http://dx.doi.org/10.1016/j.febslet.2005.08.047},
  volume       = {579},
  year         = {2005},
}