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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.

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

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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