Differentiating the effects of Cx36 and E-cadherin for proper insulin secretion of MIN6 cells.

Détails

ID Serval
serval:BIB_18B679C37EBA
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Differentiating the effects of Cx36 and E-cadherin for proper insulin secretion of MIN6 cells.
Périodique
Experimental Cell Research
Auteur(s)
Calabrese A., Caton D., Meda P.
ISSN
0014-4827[print], 0014-4827[linking]
Statut éditorial
Publié
Date de publication
2004
Volume
294
Numéro
2
Pages
379-391
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
Publication Status: ppublish
Résumé
Connexins have been implicated in many cell functions, even though in most cases it is still unclear whether these functions may actually be mediated by other proteins that are secondarily affected by connexin changes. Secretory systems provide useful models in which to tackle this central question. Primary pancreatic beta-cells and insulin-producing lines are connected by gap junction channels made of Cx36. Using stable transfection of an antisense Cx36 cDNA, we have previously obtained clones of MIN6 cells that featured a markedly reduced expression of Cx36 and impaired insulin secretion. Here, we first show that this change also resulted in loss of E-cadherin and occludin expression, thus preventing the attribution of the secretory defects to a specific type of membrane protein. To investigate this question, we have now restored the expression of either Cx36 or E-cadherin in the Cx36 antisense-transfected cells. We show that a lentivirus-mediated transduction efficiently restored Cx36 expression in MIN6 cells and allowed for expression of variable levels of this protein. We further document that adequate but not excessive levels of Cx36 allowed for recover of normal insulin secretion in response to various secretagogues. Finally, we demonstrate that restoration of normal E-cadherin expression was not able to achieve the same secretory correction. The data demonstrate that Cx36, but not E-cadherin, is necessary to control specific steps of beta-cell secretion.
Mots-clé
Animals, Cadherins/genetics, Cadherins/metabolism, Cell Adhesion/genetics, Cell Communication/genetics, Cell Line, Tumor, Connexins/genetics, Connexins/metabolism, DNA, Antisense/genetics, Dogs, Down-Regulation/genetics, Gap Junctions/genetics, Gap Junctions/metabolism, Gene Expression Regulation/genetics, Insulin/secretion, Islets of Langerhans/metabolism, Islets of Langerhans/secretion, Membrane Proteins/genetics, Membrane Proteins/metabolism, Mice, Microscopy, Electron, Scanning, Tight Junctions/genetics, Tight Junctions/metabolism, Transfection
Pubmed
Création de la notice
21/06/2010 11:38
Dernière modification de la notice
20/08/2019 13:49
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