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Connexin 36 controls synchronization of Ca2+ oscillations and insulin secretion in MIN6 cells.

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  • 2003-01-24
Published in:
  • Diabetes. - 2003
Amphotericin B
Animals
Base Sequence
Calcium Signaling
Cell Line
Connexins
DNA Primers
Electric Conductivity
Electrophysiology
Gap Junctions
Gene Expression Regulation
Glucose
Insulin
Insulin Secretion
Islets of Langerhans
Reverse Transcriptase Polymerase Chain Reaction
English Cx36 is the predominant connexin isoform expressed by pancreatic beta-cells. However, little is known about the role of this protein in the functioning of insulin-secreting cells. To address this question, we searched for a cell line expressing Cx36 and having glucose-induced insulin secretion comparable to that of primary beta-cells. By evaluating Cx36 expression in MIN6, betaTC3, RIN2A, INS1, and HIT cell lines, which differ in their sensitivity to glucose, we found that wild-type MIN6 cells fit these requirements. Therefore, we stably transfected MIN6 cells with a cDNA coding for a Cx36 antisense sequence to study the role of Cx36 in these cells. Independent clones of MIN6 cells were obtained that had a markedly reduced Cx36 expression. Loss of Cx36 decreased functional gap junctional conductance in these clones. This alteration impaired the synchronization of glucose-induced [Ca(2+)](i) oscillations and insulin secretion in response to glucose, to secretagogues that increase [cAMP](i), and to depolarizing conditions. These data provide the first evidence that Cx36-made channels 1) mediate functional coupling in MIN6 cells, 2) provide for synchronous [Ca(2+)](i) oscillations, and 3) are necessary for proper insulin secretion in response to metabolizable and nonmetabolizable secretagogues.
Language
  • English
Open access status
bronze
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Persistent URL
https://sonar.rero.ch/global/documents/5307
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