Mansouri, Ahmed

[["dc.bibliographiccitation.firstpage","3948"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","3957"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Shamsi, Farnaz"],["dc.contributor.author","Parlato, Rosanna"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T09:31:14Z"],["dc.date.available","2018-11-07T09:31:14Z"],["dc.date.issued","2014"],["dc.description.abstract","The putative induction of adult -cell regeneration represents a promising approach for the treatment of type 1 diabetes. Toward this ultimate goal, it is essential to develop an inducible model mimicking the long-lasting disease progression. In the current study, we have established a novel -cell ablation mouse model, in which the -cell mass progressively declines, as seen in type 1 diabetes. The model is based on the -cell specific genetic ablation of the transcription initiation factor 1A, TIF-IA, essential for RNA Polymerase I activity (TIF-IA(/)). Using this approach, we induced a slow apoptotic response that eventually leads to a protracted -cell death. In this model, we observed -cell regeneration that resulted in a complete recovery of the -cell mass and normoglycemia. In addition, we showed that adaptive proliferation of remaining -cells is the prominent mechanism acting to compensate for the massive -cell loss in young but also aged mice. Interestingly, at any age, we also detected -like cells expressing the glucagon hormone, suggesting a transition between - and -cell identities or vice versa. Taken together, the TIF-IA(/) mouse model can be used to investigate the potential therapeutic approaches for type 1 diabetes targeting -cell regeneration."],["dc.identifier.doi","10.4161/15384101.2014.952176"],["dc.identifier.isi","000348329600024"],["dc.identifier.pmid","25558832"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31496"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1551-4005"],["dc.relation.issn","1538-4101"],["dc.title","A genetic mouse model for progressive ablation and regeneration of insulin producing beta-cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Developmental Cell"],["dc.bibliographiccitation.lastpage","100"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Al-Hasani, Keith"],["dc.contributor.author","Pfeifer, Anja"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Ben-Othman, Nouha"],["dc.contributor.author","Gjernes, Elisabet"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Druelle, Noemie"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Ravassard, Philippe"],["dc.contributor.author","Leuckx, Gunter"],["dc.contributor.author","Lacas-Gervais, Sandra"],["dc.contributor.author","Ambrosetti, Damien"],["dc.contributor.author","Benizri, Emmanuel"],["dc.contributor.author","Hecksher-Sorensen, Jacob"],["dc.contributor.author","Gounon, Pierre"],["dc.contributor.author","Ferrer, Jorge"],["dc.contributor.author","Gradwohl, Gerard"],["dc.contributor.author","Heimberg, Harry"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.date.accessioned","2018-11-07T09:22:22Z"],["dc.date.available","2018-11-07T09:22:22Z"],["dc.date.issued","2013"],["dc.description.abstract","It was recently demonstrated that embryonic glucagon-producing cells in the pancreas can regenerate and convert into insulin-producing beta-like cells through the constitutive/ectopic expression of the Pax4 gene. However, whether alpha cells in adult mice display the same plasticity is unknown. Similarly, the mechanisms underlying such reprogramming remain unclear. We now demonstrate that the misexpression of Pax4 in glucagon(+) cells age-independently induces their conversion into beta-like cells and their glucagon shortage-mediated replacement, resulting in islet hypertrophy and in an unexpected islet neogenesis. Combining several lineage-tracing approaches, we show that, upon Pax4-mediated alpha-to-beta-like cell conversion, pancreatic duct-lining precursor cells are continuously mobilized, re-express the developmental gene Ngn3, and successively adopt a glucagon+ and a beta-like cell identity through a mechanism involving the reawakening of the epithelial-to-mesenchymal transition. Importantly, these processes can repeatedly regenerate the whole beta cell mass and thereby reverse several rounds of toxin-induced diabetes, providing perspectives to design therapeutic regenerative strategies."],["dc.identifier.doi","10.1016/j.devcel.2013.05.018"],["dc.identifier.isi","000322087400009"],["dc.identifier.pmid","23810513"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29326"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","1534-5807"],["dc.title","Adult Duct-Lining Cells Can Reprogram into beta-like Cells Able to Counter Repeated Cycles of Toxin-Induced Diabetes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","838"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Seminars in Cell and Developmental Biology"],["dc.bibliographiccitation.lastpage","844"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Heimberg, Harry"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T08:38:58Z"],["dc.date.available","2018-11-07T08:38:58Z"],["dc.date.issued","2010"],["dc.description.abstract","The pancreas is composed of two main compartments consisting of endocrine and exocrine tissues. The majority of the organ is exocrine and responsible for the synthesis of digestive enzymes and for their transport via an intricate ductal system into the duodenum. The endocrine tissue represents less than 2% of the organ and is organized into functional units called islets of Langerhans, comprising alpha-, beta-, delta-, epsilon- and PP-cells, producing the hormones glucagon, insulin, somatostatin, ghrelin and pancreatic polypeptide (PP), respectively. Insulin-producing beta- cells play a central role in the control of the glucose homeostasis. Accordingly, absolute or relative deficiency in beta-cells may ultimately lead to type 1 and/or type 2 diabetes, respectively. One major goal of diabetes research is therefore to understand the molecular mechanisms controlling the development of beta-cells during pancreas morphogenesis, but also those underlying the regeneration of adult injured pancreas, and assess their significance for future cell-based therapy. In this review, we will therefore present new insights into beta-cell development with focus on beta-cell regeneration. (C) 2010 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.semcdb.2010.07.007"],["dc.identifier.isi","000283598400010"],["dc.identifier.pmid","20688184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18878"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.issn","1084-9521"],["dc.title","Pancreatic beta-cells: From generation to regeneration"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3450"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","3451"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T11:22:28Z"],["dc.date.available","2018-11-07T11:22:28Z"],["dc.date.issued","2009"],["dc.description.sponsorship","NIDDK NIH HHS [U19 DK 072495-01]"],["dc.identifier.doi","10.4161/cc.8.21.9791"],["dc.identifier.isi","000272218600009"],["dc.identifier.pmid","19838059"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55998"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1538-4101"],["dc.title","Turning on the beta-cell identity in the pancreas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4299"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","4311"],["dc.bibliographiccitation.volume","216"],["dc.contributor.author","Druelle, Noémie"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Shabro, Aidin"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Mondin, Magali"],["dc.contributor.author","Rekima, Samah"],["dc.contributor.author","Napolitano, Tiziana"],["dc.contributor.author","Silvano, Serena"],["dc.contributor.author","Navarro-Sanz, Sergi"],["dc.contributor.author","Hadzic, Biljana"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Rassoulzadegan, Minoo"],["dc.contributor.author","Schmid, Herbert A."],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.date.accessioned","2020-12-10T18:15:35Z"],["dc.date.available","2020-12-10T18:15:35Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1083/jcb.201704044"],["dc.identifier.eissn","1540-8140"],["dc.identifier.issn","0021-9525"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74895"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Ectopic expression of Pax4 in pancreatic δ cells results in β-like cell neogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","449"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell"],["dc.bibliographiccitation.lastpage","462"],["dc.bibliographiccitation.volume","138"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Ravassard, Philippe"],["dc.contributor.author","Sosa-Pineda, Beatriz"],["dc.contributor.author","Dussaud, Sebastien"],["dc.contributor.author","Billestrup, Nils"],["dc.contributor.author","Madsen, Ole D."],["dc.contributor.author","Serup, Palle"],["dc.contributor.author","Heimberg, Harry"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T11:25:44Z"],["dc.date.available","2018-11-07T11:25:44Z"],["dc.date.issued","2009"],["dc.description.abstract","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 alpha cells, to adopt a beta cell destiny. This results in a glucagon deficiency that provokes a compensatory and continuous glucagon(+) cell neogenesis requiring the re-expression of the pro-endocrine gene Ngn3. However, the newly formed alpha cells fail to correct the hypoglucagonemia since they subsequently acquire a beta cell phenotype upon Pax4 ectopic expression. Notably, this cycle of neogenesis and redifferentiation caused by ectopic expression of Pax4 in alpha cells is capable of restoring a functional beta cellmass and curing diabetes in animals that have been chemically depleted of beta cells."],["dc.identifier.doi","10.1016/j.cell.2009.05.035"],["dc.identifier.isi","000268771900011"],["dc.identifier.pmid","19665969"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56693"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","0092-8674"],["dc.title","The Ectopic Expression of Pax4 in the Mouse Pancreas Converts Progenitor Cells into alpha and Subsequently beta Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","763"],["dc.bibliographiccitation.issue","8-9"],["dc.bibliographiccitation.journal","médecine/sciences"],["dc.bibliographiccitation.lastpage","765"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T08:27:24Z"],["dc.date.available","2018-11-07T08:27:24Z"],["dc.date.issued","2009"],["dc.identifier.doi","10.1051/medsci/2009258-9763"],["dc.identifier.isi","000270258100023"],["dc.identifier.pmid","19765395"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16198"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Editions Edk"],["dc.relation.issn","0767-0974"],["dc.title","Pax4 transdifferentiates glucagon-secreting alpha cells to insulin-secreting beta endocrine pancreatic cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]