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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 continuous low-grade inflammation

AutorRodríguez-Gallego, Esther; Corbí, Angel L. ; Sierra-Filardi, Elena ; Joven, Jorge
Fecha de publicación15-oct-2013
EditorHindawi Publishing Corporation
CitaciónMediators of Inflammation Volume 2013, Article ID 953841, 19 pages
ResumenExcessive 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. © 2013 Esther Rodríguez-Gallego et al.
DescripciónRodríguez-Gallego, Esther [et alt.]; 20 p.-11 fig.
Versión del editorhttp://dx.doi.org/10.1155/2013/953841
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