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Pedro Herrera

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Prof. Pedro Herrera

Destin cellulaire et spécification des cellules pancréatiques

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Pedro Herrera obtient un master en biologie de l’université Complutense de Madrid en 1985. En 1994, il obtient un doctorat ès sciences de l’université de Genève et devient, en 1996, chercheur indépendant au sein du département de morphologie de la Faculté de médecine, avec le soutien de la Juvenile Diabetes Research Foundation, puis du FNS. Il est nommé maître d’enseignement et de recherche en 2000, professeur adjoint au sein du Département de médecine génétique et développement en 2009, puis professeur ordinaire en décembre 2013. En produisant des souris transgéniques, il publie le premier traçage génétique de lignages cellulaires in vivo chez un embryon de mammifère. Ses travaux, dans les domaines du développement embryonnaire et la régénération, portent sur l’origine des cellules à insuline et visent à développer des traitements innovants du diabète.

Research aims

Prof. Herrera's group studies the genetic regulation of pancreas development and, more extensively, of pancreas regeneration after injury. We produce and use different transgenic mice to address biological questions related to the regeneration of insulin-producing beta-cells in diabetic situations.

Using an in vivo clonal cell lineage tracing analysis, in 2009, they found that pancreatic Neurogenin3-expressing cells, which were believed to be multipotent precursors to all pancreatic islet endocrine cell types during development, are strictly unipotent at the single cell level (Desgraz & Herrera, 2009).

In the field of regenerative biology,they have discovered that adult mice retain the ability to generate new beta-cells when they become diabetic; this is possible because there is a high degree of cell plasticity, since the majority of the reconstituted insulin-producing cells in a situation of extreme beta-cell loss are indeed naturally reprogrammed glucagon-producing alpha-cells, and somatostatin-producing delta-cells (Thorel et al, 2010; Chera et al, 2014). These processes of “a-to-b” and “d-to-b” direct conversion without proliferation (termed transdifferentiation) involve a minority of a- and d-cells. In juvenile mice, however, they have observed an astonishingly rapid and efficient diabetes recovery after near total beta-cell ablation, yet through a completely different cell fate change (“transfating”) mechanism: the massive indirect reprogramming of delta-cells into insulin producers, by a process of dedifferentiation, proliferation and redifferentiation (Chera et al, 2014). Understanding the nature of these spontaneous forms of intra-islet cell conversion could provide new opportunities for fostering regenerative therapeutic approaches to treat diabetes.


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