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DIRECtA SIGNED

Targeting the Endocannabinoid System within Islets of Langerhans to Protect against Immune Destruction.

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 DIRECtA project word cloud

Explore the words cloud of the DIRECtA project. It provides you a very rough idea of what is the project "DIRECtA" about.

patients    reactivity    proposes    model    prolonged    life    function    strategy    signalling    exogenous    mass    purpose    diabetic    pancreas    progressive    cells    challenged    islets    alters    blockade    absolute    reported    additionally    preventing    insulitis    damage    develops    synergy    autophagy    prevalence    risk    cure    themselves    diseases    t1d    beneficial    glucose    reducing    uncontrolled    manipulation    cannabidiol    antagonist    immune    beta    endocannabinoid    modulating    treating    disease    producing    knockout    insulin    activation    spontaneously    levels    preserving    inflammatory    renal    cb2    inflammation    europe    cardiovascular    gpr55    action    autoimmune    metabolism    destruction    children    intend    secretion    ecrs    proliferation    regulators    prevented    receptors    interaction    mice    play    thereby    protecting    cell    incidence    mitochondrial    langerhans    mouse    administration    infections    generate    diabetes    infiltration    highest    neuropathy    blood    ameliorated    obese    therapies    pharmacological    peripheral    cb1    capita   

Project "DIRECtA" data sheet

The following table provides information about the project.

Coordinator
FUNDACION PUBLICA ANDALUZA PARA LA INVESTIGACION DE MALAGA EN BIOMEDICINA Y SALUD 

Organization address
address: CALLE DOCTOR MIGUEL DIAZ RECIO 28 PLANTA BAJA
city: MALAGA
postcode: 29010
website: n.a.

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Spain [ES]
 Total cost 158˙121 €
 EC max contribution 158˙121 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-01-03   to  2020-01-02

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FUNDACION PUBLICA ANDALUZA PARA LA INVESTIGACION DE MALAGA EN BIOMEDICINA Y SALUD ES (MALAGA) coordinator 158˙121.00

Map

 Project objective

Europe has the highest prevalence per capita of children with type 1 diabetes (T1D), an autoimmune disease with no cure that results in progressive destruction, and finally an absolute loss, of insulin-producing beta (β) cells in islets of Langerhans in the pancreas. This means that patients require exogenous insulin administration for life. Additionally, prolonged uncontrolled blood glucose levels increase the risk of cardiovascular diseases, peripheral neuropathy, renal failure and numerous infections. The endocannabinoid receptors (ECRs) CB1, CB2 and GPR55 are regulators of metabolism and immune action and are also present on β cells. Cannabidiol, a CB1 antagonist, reduced the incidence of T1D in mice by reducing insulitis, thereby preserving β cell mass. Additionally, blockade of CB1 alters insulin secretion, increasing proliferation and autophagy in β cells. Importantly, β cell-specific CB1 knockout mice have no T-cell infiltration in islets when their pancreas is challenged. Furthermore, activation of GPR55 and CB2 are reported to be beneficial in protecting from inflammation. In this project we intend to study the interaction of the ECRs and their potential synergy for protecting β cells from insulitis. For this purpose, we will generate a non-obese diabetic (spontaneously develops autoimmune insulitis) β cell-specific CB1 knockout mouse, and use pharmacological approaches to enhance GPR55 and CB2 signalling to determine if the diabetic condition can be prevented/ameliorated. We will assess β cell damage together with mitochondrial function, autophagy, and inflammatory responses in our mouse model and after pharmacological manipulation. Thus, this project proposes a new strategy, not focusing on the immune system but on the role that β cells themselves play in modulating their own reactivity, for the development of new therapies for preventing and/or treating T1D.

 Publications

year authors and title journal last update
List of publications.
2020 Silvana Y. Romero-Zerbo, María García-Fernández, Vanesa Espinosa-Jimenez, Macarena Pozo-Morales, Alejandro Escamilla-Sánchez, Lourdes Sánchez-Salido, Estrella Lara, Nadia Cobo-Vuilleumier, Alex Rafacho, Gabriel Olveira, Gemma Rojo-Martínez, Benoit R. Gauthier, Isabel González-Mariscal and Francisco J. Bermúdez-Silva
THE ATYPICAL CANNABINOID ABN-CBD REDUCES INFLAMMATION AND PROTECTS LIVER, PANCREAS AND ADIPOSE TISSUE IN A MOUSE MODEL OF PREDIABETES AND NON-ALCOHOLIC FATTY LIVER DISEASE
published pages: , ISSN: 1664-2392, DOI: 10.3389/fendo.2020.00103
Frontiers in Endocrinology 2020-03-05

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