EMPANMES

Cellular composition of the pancreas: elucidating the role of mesenchymal signaling pathways

Coordinatore	TEL AVIV UNIVERSITY    more  Organization address address: RAMAT AVIV city: TEL AVIV postcode: 69978 contact info Titolo: Ms. Nome: Lea Cognome: Pais Email: send email Telefono: 97236408774 Fax: 97236409697
Nazionalità Coordinatore	Israel [IL]
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2012-CIG
Funding Scheme	MC-CIG
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-03-01   -   2017-02-28

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	TEL AVIV UNIVERSITY  Organization address address: RAMAT AVIV city: TEL AVIV postcode: 69978 contact info Titolo: Ms. Nome: Lea Cognome: Pais Email: send email Telefono: 97236408774 Fax: 97236409697	IL (TEL AVIV)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'The pancreas constitutes of various cell types with distinctive function. Exocrine cells produce and secrete digestive enzymes while endocrine cells, including insulin-producing beta-cells, secrete hormones that regulate glucose homeostasis. The proportional quantity of the different pancreatic cell populations is well defined, when exocrine cells encompass majority of the tissue mass. However, while the establishment of pancreas cellular composition during embryogenesis has been well acknowledged, its regulation is far from being elucidated. While cell intrinsic cues were shown to influent this process in the developing pancreas, the role of extrinsic signals is less understood. I hypothesize that extrinsic cues define the rate of cell proliferation and therefore govern the sizes of various pancreatic cell populations in vivo. Here I will use a novel transgenic mouse model I have recently developed, the Nkx3.2-Cre mouse line, as a tool to evaluate extrinsic roles in the regulation of pancreas cellular composition. I will further use this tool to elucidate the extrinsic cues playing a role in this process. To this end, I will deregulate signaling pathways in the pancreatic mesenchyme, a key component of the embryonic pancreas microenvironment. I will focus on two such pathways, the Hedgehog and the Wnt pathways, which are required for normal mesenchymal gene expression. I expect their deregulation will hamper mesenchymal ability to promote appropriate pancreatic cellular composition, and will enable the identification of extrinsic cues required for this process. The findings of this study will allow better understanding of the extrinsic requirements during pancreas development, and the cues governing its cellular composition. Furthermore, this study will aid current affords to expand beta-cells upon will, as a potential cure to diabetes.'