西亚试剂：The Ectopic Expression of Pax4 in the Mouse Pancreas Conver

The Ectopic Expression of Pax4 in the Mouse Pancreas Converts Progenitor Cells into  and Subsequently  Cells

Patrick Collombat1,2,3,11,,,Xiaobo Xu4,Philippe Ravassard3,5,Beatriz Sosa-Pineda6,Sébastien Dussaud5,7,Nils Billestrup8,Ole D. Madsen2,3,9,Palle Serup2,3,9,Harry Heimberg2,3,4andAhmed Mansouri1,2,10,,

1 Department of Molecular Cell Biology, Max-Planck Institute for Biophysical Chemistry, Am Fassberg, D-37077 G?ttingen, Germany
2 Beta Cell Biology Consortium, 2213 Garland Avenue, 9465 MRB IV, Nashville, TN 37323-0494, USA
3 JDRF Center for Beta Cell Therapy in Diabetes, Laarbeeklaan 103, B-1090 Brussels, Belgium
4 Diabetes Research Center, Vrije Universiteit Brussel, Laarbeeklaan 103, B-1090 Brussels, Belgium
5 Biotechnology and Biotherapy Laboratory, Centre de Recherche de l'Institut du Cerveau et de la Moelle, CNRS UMR 7225, INSERM UMRS 975, University Pierre et Marie Curie, H?pital Pitié Salpêtrière, FR-75013 Paris, France
6 Department of Genetics/Tumor Cell Biology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105-3678, USA
7 Centre d'Expérimentation Fonctionnelle, Pitié Salpêtrière Medical Faculty, Université Pierre et Marie Curie, FR-75013 Paris, France
8 Department of Translational Diabetology Research Institute, Hagedorn Niels Steensensvej 6, DK-2820 Gentofte, Denmark
9 Department of Developmental Biology Research Institute, Hagedorn Niels Steensensvej 6, DK-2820 Gentofte, Denmark
10 Department of Clinical Neurophysiology, University of Göttingen, Robert-Koch Strasse 40, D-37075 G?ttingen, Germany

We have previously reported that the loss of Arx and/or Pax4 gene activity leads to a shift in the fate of the different endocrine cell subtypes in the mouse pancreas, without affecting the total endocrine cell numbers. Here, we conditionally and ectopically express Pax4 using different cell-specific promoters and demonstrate that Pax4 forces endocrine precursor cells, as well as mature α cells, to adopt a β cell destiny. This results in a glucagon deficiency that provokes a compensatory and continuous glucagon+ cell neogenesis requiring the re-expression of the proendocrine gene Ngn3. However, the newly formed β cells fail to correct the hypoglucagonemia since they subsequently acquire a β cell phenotype upon Pax4 ectopic expression. Notably, this cycle of neogenesis and redifferentiation caused by ectopic expression of Pax4 in β cells is capable of restoring a functional β cell mass and curing diabetes in animals that have been chemically depleted of β cells.

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