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Adenovirus‐mediated silencing of Synaptotagmin 9 inhibits Ca 2+ ‐dependent insulin secretion in islets
Author(s) -
Iezzi Mariella,
Eliasson Lena,
Fukuda Mitsunori,
Wollheim Claes B.
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.08.047
Subject(s) - islet , secretion , gene silencing , insulin , synaptotagmin 1 , chemistry , microbiology and biotechnology , pancreatic islets , endocrinology , medicine , biology , vesicle , biochemistry , gene , synaptic vesicle , membrane
Synaptotagmins (Syts) are involved in Ca 2+ ‐dependent insulin release. However, which Syt isoform is functional in primary β‐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 β‐cell secretion.