Activation of NF-κB by Extracellular Matrix Is Involved in Spreading and Glucose-stimulated Insulin Secretion of Pancreatic Beta Cells
作者： Eva B. Hammar , Jean-Claude Irminger , Katharina Rickenbach , Géraldine Parnaud , Pascale Ribaux
关键词: Internal medicine 、 Alpha (ethology) 、 Integrin 、 Cell biology 、 Cell nucleus 、 Endocrinology 、 Biology 、 Actin cytoskeleton organization 、 Extracellular matrix 、 Phosphorylation 、 NF-κB 、 Beta cell
摘要: Laminin-5-rich extracellular matrix derived from 804G cells (804G-ECM) engages beta1 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 NF-kappaB involvement in those effects on induces nuclear translocation DNA binding p65 subunit NF-kappaB. 804G-ECM-induced was weak as compared with that induced by interleukin-1beta. Transient (peak at 2 h) overexpression target genes IkappaB alpha NF-kappaB1(p105) 4 were observed. When inhibited an inhibitor phosphorylation (Bay 11-7082) or a recombinant adenovirus expressing nonphosphorylatable form alpha, cell spreading actin cytoskeleton organization reduced. GSIS 5-fold, whereas not affected. In summary, results indicate transient moderate activity. This shows for first time ECM-induced is necessary maintaining GSIS, although it does affect contrast deleterious cytokine-induced It proposed essential proper function cell.
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