Coordinatore | KAROLINSKA INSTITUTET
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
Nazionalità Coordinatore | Sweden [SE] |
Totale costo | 2˙499˙590 € |
EC contributo | 2˙499˙590 € |
Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
Code Call | ERC-2013-ADG |
Funding Scheme | ERC-AG |
Anno di inizio | 2014 |
Periodo (anno-mese-giorno) | 2014-03-01 - 2019-02-28 |
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1 |
KAROLINSKA INSTITUTET
Organization address
address: Nobels Vag 5 contact info |
SE (STOCKHOLM) | hostInstitution | 2˙499˙590.00 |
2 |
KAROLINSKA INSTITUTET
Organization address
address: Nobels Vag 5 contact info |
SE (STOCKHOLM) | hostInstitution | 2˙499˙590.00 |
Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.
'The challenge in cell physiology/pathology today is to translate in vitro findings to the living organism. We have developed a unique approach where signal-transduction can be investigated in vivo non-invasively, longitudinally at single cell resolution, using the anterior chamber of the eye as a natural body window for imaging. We will use this approach to understand how the universally important and highly complex signal Ca2 is regulated in the pancreatic beta-cell, while localized in the vascularized and innervated islet of Langerhans, and how that affects the insulin secretory machinery in vivo. Engrafted islets in the eye take on identical innervation- and vascularization patterns as those in the pancreas and are proficient in regulating glucose homeostasis in the animal. Since the pancreatic islet constitutes a micro-organ, this imaging approach offers a seminal model system to understand Ca2 signaling in individual cells at the organ level in real life. We will test the hypothesis that the Ca2-signal has a key role in pancreatic beta-cell function and survival in vivo and that perturbation in the Ca2-signal serves as a common denominator for beta-cell pathology associated with impaired glucose homeostasis and diabetes. Of special interest is how innervation impacts on Ca2-dynamics and the integration of autocrine, paracrine and endocrine signals in fine-tuning the Ca2-signal with regard to beta-cell function and survival. We aim to define key defects in the machinery regulating Ca2-dynamics in association with the autoimmune reaction, inflammation and obesity eventually resulting in diabetes. Our imaging platform will be applied to clarify in vivo regulation of Ca2-dynamics in both healthy and diabetic human beta-cells. To define novel drugable targets for treatment of diabetes, it is crucial to identify similarities and differences in the molecular machinery regulating the in vivo Ca2-signal in the human and in the rodent beta-cell.'