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Articles by G Parnaud
Total Records ( 3 ) for G Parnaud
  G Parnaud , E Hammar , P Ribaux , M. Y Donath , T Berney and P. A. Halban

Laminin-5-rich extracellular matrix derived from 804G cells (804G-ECM) induces spreading, improves glucose-stimulated insulin secretion, and increases survival and proliferation of rat pancreatic β-cells. The aim of the study was to determine growth signaling pathways activated by ECM with a particular focus on Ca2+-dependent transcription factors. 804G-ECM increased rat β-cell proliferation, and this stimulation was glucose and Ca2+ dependent. NF-B nuclear translocation as well as IB gene expression were also Ca2+ dependent. Inhibition of NF-B almost completely blocked 804G-ECM-stimulated β-cell proliferation as did the soluble IL-1 receptor antagonist IL-1Ra. 804G-ECM-induced proliferation was also blocked by cyclosporin A and the VIVIT peptide, suggesting involvement of nuclear factor of activated T cells (NFAT)/calcineurin. Use of selective inhibitors further implicated other pathways in this process. Inhibition of phosphatidylinositol 3-kinase and protein kinase A both prevented β-cell replication stimulated by 804G-ECM. Conversely, inhibition of MAPK, c-Jun N-terminal kinase, p38, and glycogen synthase kinase-3β increased β-cell proliferation on 804G-ECM. Our results suggest that Ca2+ entry, which is necessary for increased β-cell proliferation on 804G-ECM, is also involved in 804G-ECM-induced NF-B activity. It is proposed that increased cytosolic Ca2+ leads to activation of the transcription factors NFAT and NF-B that in turn increase β-cell proliferation. Activation of phosphatidylinositol 3-kinase by 804G-ECM also increases proliferation possibly by synergistic coactivation of NFAT via inhibition of glycogen synthase kinase-3β, whereas IL-1β may amplify the process by feed-forward activation of NF-B. Conversely, inhibition of the MAPK pathway increased β-cell proliferation, indicating a counterregulatory restraining role for this signaling pathway.

  B Kutlu , A. G Kayali , S Jung , G Parnaud , D Baxter , G Glusman , N Goodman , L. A Behie , A Hayek and L. Hood

Pancreatic islet transplantation as a potential cure for type 1 diabetes (T1D) cannot be scaled up due to a scarcity of human pancreas donors. In vitro expansion of β-cells from mature human pancreatic islets provides an alternative source of insulin-producing cells. The exact nature of the expanded cells produced by diverse expansion protocols and their potential for differentiation into functional β-cells remain elusive. We performed a large-scale meta-analysis of gene expression in human pancreatic islet cells, which were processed using three different previously described protocols for expansion and for which redifferentiation was attempted. All three expansion protocols induced dramatic changes in the expression profiles of pancreatic islets; many of these changes are shared among the three protocols. Attempts at redifferentiation of expanded cells induce a limited number of gene expression changes. Nevertheless, these fail to restore a pancreatic islet-like gene expression pattern. Comparison with a collection of public microarray datasets confirmed that expanded cells are highly comparable to mesenchymal stem cells. Genes induced in expanded cells are also enriched for targets of transcription factors important for pluripotency induction. The present data increase our understanding of the active pathways in expanded and redifferentiated islets. Knowledge of the mesenchymal stem cell potential may help development of drug therapeutics to restore β-cell mass in T1D patients.

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