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J. Biol. Chem., Vol. 280, Issue 34, 30630-30637, August 26, 2005
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Activation of NF-
B by Extracellular Matrix Is Involved in Spreading and Glucose-stimulated Insulin Secretion of Pancreatic Beta Cells*
From the
Department of Genetic Medicine and Development, University Medical Center and ¶Cell Isolation and Transplantation Center, University Hospital, 1211 Geneva 4, Switzerland
Laminin-5-rich extracellular matrix derived from 804G cells (804G-ECM) engages 
1 integrins to induce spreading, improve glucose-stimulated insulin secretion (GSIS), and increase survival of pancreatic beta cells. The present study examines whether 804G-ECM activates the transcriptional activity of NF-
B and the involvement of NF-B in those effects of 804G-ECM on pancreatic beta cells. 804G-ECM induces nuclear translocation and the DNA binding activity of the p65 subunit of NF-B. 804G-ECM-induced nuclear translocation of NF-B was weak as compared with that induced by interleukin-1. Transient 804G-ECM-induced DNA binding activity of NF-B (peak at 2 h) and overexpression of NF-B target genes IB
and NF-B1(p105) (peak at 4 h) were observed. When NF-B was inhibited by an inhibitor of IB phosphorylation (Bay 11-7082) or by a recombinant adenovirus expressing the nonphosphorylatable form of IB, 804G-ECM-induced cell spreading and actin cytoskeleton organization were reduced. GSIS from cells on 804G-ECM was inhibited 5-fold, whereas cell survival was not affected. In summary, the results indicate that 804G-ECM induces a transient and moderate NF-B activity. This study shows for the first time that ECM-induced NF-B activity is necessary in maintaining GSIS, although it does not affect survival of pancreatic beta cells. The effects of ECM-induced NF-B activity contrast with the deleterious effects of cytokine-induced NF-B activity. It is proposed that transient and moderate NF-B activity is essential for proper function of the pancreatic beta cell.
Received for publication, March 7, 2005 , and in revised form, May 31, 2005.
* This work was supported by Grant 3200-06177.00 from the Swiss National Science Foundation, Grant 4-2002-461 from the Juvenile Diabetes Research Foundation, and an unrestricted educational grant from Novo Nordisk A/S, Copenhagen. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Genetic Medicine and Development, University Medical Center, Rue Michel Servet 1, 1211 Geneva 4, Switzerland. Tel.: 41-22-379-5537; Fax: 41-22-379-5528; E-mail: eva.hammar{at}medecine.unige.ch.
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