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Título: | Osteoarticular Expression of Musashi-1 in an Experimental Model of Arthritis |
Autor: | O’Valle, Francisco; Peregrina, Magdalena; Crespo-Lora, Vicente; Galindo-Moreno, Pablo; Roman, María; Padial-Molina, Miguel; Mesa, Francisco; Aneiros-Fernández, J.; Aguilar, David CSIC ORCID; González-Rey, Elena CSIC ORCID; Delgado, M.; Hernández-Cortés, Pedro | Fecha de publicación: | 2015 | Editor: | Hindawi Publishing Corporation | Citación: | BioMed Research International | Resumen: | Background. Collagen-induced arthritis (CIA), a murine experimental disease model induced by immunization with type II collagen (CII), is used to evaluate novel therapeutic strategies for rheumatoid arthritis. Adult stem cell marker Musashi-1 (Msi1) plays an important role in regulating themaintenance and differentiation of stem/precursor cells.The objectives of this investigation were to performa morphological study of the experimental CIAmodel, evaluate the effect of TNF-blocker (etanercept) treatment, and determine the immunohistochemical expression of Msi1 protein. Methods. CIA was induced in 50 male DBA1/J mice for analyses of tissue and serum cytokine; clinical and morphological lesions in limbs; and immunohistochemical expression of Msi1. Results. Clinically, TNF-blocker treatment attenuated CIA on day 32 after immunization (p < 0.001). Msi1 protein expression was significantly higher in joints damaged by CIAthan in those with no lesions (p < 0.0001) and was related to the severity of the lesions (Spearman’s rho = 0.775, p = 0.0001). Conclusions. Treatment with etanercept attenuates osteoarticular lesions in the murine CIA model. Osteoarticular expression of Msi1 protein is increased in joints with CIA-induced lesion and absent in nonlesioned joints, suggesting that this protein is expressed when the lesion is produced in order to favor tissue repair. | Versión del editor: | http://www.hindawi.com/journals/bmri/2015/681456/ | URI: | http://hdl.handle.net/10261/133768 | DOI: | 10.1155/2015/681456 | ISSN: | 2314-6133 | E-ISSN: | 2314-6141 |
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