Osteoarticular Expression of Musashi-1 in an Experimental Model of Arthritis
Identificadores
URI: http://hdl.handle.net/10481/36639DOI: 10.1155/2015/681456
ISSN: 2314-6133
ISSN: 2314-6141
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O'Valle Ravassa, Francisco Javier; Peregrina Palomares, Mª Magdalena; Crespo-Lora, Vicente; Galindo Moreno, Pablo Antonio; Roman, María; Padial Molina, Miguel; Mesa Aguado, Francisco Luis; Hernández-Cortés, PedroEditorial
Hindawi Publishing Corporation
Materia
Collagen-induced arthritis (CIA) Arthritis Rheumatoid arthiritis Stem cells Tissue repair
Date
2015Referencia bibliográfica
O'Valle, F.; et al. Osteoarticular Expression of Musashi-1 in an Experimental Model of Arthritis. BioMed Research International, 2015: 681456 (2015). [http://hdl.handle.net/10481/36639]
Sponsorship
This investigation was partially supported by Research Group #CTS-138 (Junta de Andalucía, Spain).Abstract
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 the maintenance and differentiation of stem/precursor cells. The objectives of this investigation were to perform a morphological study of the experimental CIA model, evaluate the effect of TNFα-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, TNFα-blocker treatment attenuated CIA on day 32 after immunization (). Msi1 protein expression was significantly higher in joints damaged by CIA than in those with no lesions () and was related to the severity of the lesions (Spearman’s rho = 0.775, ). 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.