Pedro Herrera, Ph.D. - Investigator Profile
Pedro L. Herrera acquired his undergraduate biology training in the University Complutense (Madrid, Spain). He received his PhD in 1994, from the University of Geneva, Faculty of Sciences (Switzerland), under the guidance of Jean-Dominique Vassalli. In 1996 he became an independent investigator at the Faculty of Medicine of Geneva after obtaining his first regular grant award from the Juvenile Diabetes Research Foundation. Today he is associate professor at the Faculty of Medicine as well as President of the University’s Animal Ethics Committee, and Director of its Transgenic Core Facility. He is member of several international scientific committees.
Pedro investigates pancreas development, cell lineage allocation during pancreatic ontogeny, and adult pancreas regeneration using different transgenic mouse models. He pioneered the study of mouse pancreas development and carried out the first in vivo ablation of different pancreatic endocrine cell types during his thesis (Herrera et al, 1991; Herrera et al, 1994). Later, he performed the first in vivo cell lineage tracing analysis using the Cre/loxP system (Herrera, 2000), and demonstrated the existence of competence windows for beta-catenin signaling in exocrine cells during pancreatic growth (Strom et al., 2007). He has found that adult acinar cells can transdifferentiate to adipocytes with ageing and in certain pathological conditions (Bonal et al., 2009), thus seeding new light on the origin of adipose tissue and adult cell plasticity. More recently, he showed that pancreatic Neurogenin3-expressing cells, which are the precursors to all islet endocrine cell types, are strictly unipotent at the single cell level in vivo (Desgraz & Herrera, 2009). In the field of regenerative biology, he has found that the adult pancreas retains the ability of making new b-cells after their total or near total loss, and that this process reveals a high degree of cell plasticity, since the majority of the regenerated b-cells are indeed fully mature adult a-cells that have spontaneously reprogrammed to producing insulin and other b-cell-specific factors in this situation of extreme b-cell loss (Thorel et al, 2010).
pancreas development; beta cell development and generation; regeneration; reprogramming; cell tracing; transgenic mice