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Ubiquitous transgenic overexpression of C-C Chemokine Ligand 2: A model to Assess the Combined Effect of High Energy Intake and Continous Low-Grade Inflammation - PC:586

URV's Author/s:Esther Rodríguez-Gallego, Marta Riera-Borrull, Anna Hernández-Aguilera,Roger Mariné-Casadó, Anna Rull, Raúl Beltrán-Debón,Fedra Luciano-Mateo, Javier A. Menendez, Alejandro Vazquez-Martin, Juan J. Sirvent,Vicente Martín-Paredero, Angel L. Corbí, Elena Sierra-Filardi, Gerard Aragonès, Anabel García-Heredia, Jordi Camps, Carlos Alonso-Villaverde, Jorge Joven
Author, as appears in the article.:Joven, J.
Alonso-Villaverde, C.
Camps, J.
Garcia-Heredia, A.
Aragones, G.
Sierra-Filardi, E.
Corbi, A.
Martin Paredero, V.
Sirvent, J.
Vazquez-Martin, A.
Menendez, J.
Luciano, F.
Beltran, R.
Rull, A.
Mariné, R.
Hernandez-Aguilera, A.
Riera, M.
Rodriguez-Gallego, E.
Journal publication year:2013
ISSN:0962-9351
e-ISSN:1466-1861
Abstract:Excessive energy management leads to low-grade, chronic inflammation, which is a significant factor predicting noncommunicable diseases. In turn, inflammation, oxidation, and metabolism are associated with the course of these diseases; mitochondrial dysfunction seems to be at the crossroads of mutual relationships. The migration of immune cells during inflammation is governed by the interaction between chemokines and chemokine receptors. Chemokines, especially C-C-chemokine ligand 2 (CCL2), have a variety of additional functions that are involved in the maintenance of normal metabolism. It is our hypothesis that a ubiquitous and continuous secretion of CCL2 may represent an animal model of low-grade chronic inflammation that, in the presence of an energy surplus, could help to ascertain the afore-mentioned relationships and/or to search for specific therapeutic approaches. Here, we present preliminary data on a mouse model created by using targeted gene knock-in technology to integrate an additional copy of the CCl2 gene in the Gt(ROSA)26Sor locus of the mouse genome via homologous recombination in embryonic stem cells. Short-term dietary manipulations were assessed and the findings include metabolic disturbances, premature death, and the manipulation of macrophage plasticity and autophagy. These results raise a number of mechanistic questions for future study.
Article's DOI:http://dx.doi.org/10.1155/2013/953841
Link to the original source:http://www.hindawi.com/journals/mi/2013/953841/
Paper version:info:eu-repo/semantics/publishedVersion
licence for use:https://creativecommons.org/licenses/by/3.0/es/
Department:Bioquímica i Biotecnologia
Medicina i Cirurgia
Ciències Mèdiques Bàsiques
Licence document URL:https://repositori.urv.cat/ca/proteccio-de-dades/
Entity:Universitat Rovira i Virgili.
First page:1
Last page:18
Journal volume:2013
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