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NUCB2/nesfatin-1: a new adipokine expressed in human and murine chondrocytes with pro-inflammatory properties, an in vitro study

Scotece, Morena; Conde Aranda, Javier; Abella Cajigal, Vanesa; Rodríguez López, Verónica; Lago Paz, Francisca; Pino Mínguez, Jesús; Gómez-Reino Carnota, Juan Jesús; Gualillo ., Oreste
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URI: http://hdl.handle.net/20.500.11940/6543
PMID: 24464950
DOI: 10.1002/jor.22585
ISSN: 0736-0266
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Texto completo disponible por cortesía de Orthop Res . 2014 May;32(5):653-60. doi: 10.1002/jor.22585. (885.6Kb)
Fecha de publicación
2014
Título de revista
JOURNAL OF ORTHOPAEDIC RESEARCH
Tipo de contenido
Artigo
MeSH
Animals | Calcium-Binding Proteins | Cell Differentiation | Cell Line | Cells, Cultured | Chemokine CCL3 | Chondrocytes | Cytokines | DNA-Binding Proteins | Humans | Interleukin-6 | Interleukin-8 | Mice | Nerve Tissue Proteins | Nucleobindins | RNA, Messenger | Nucb2 | Nesfatin-1 | chondrocytes
Resumen
Nesfatin-1 is a recently discovered satiety-inducing adipokine identified in hypothalamic regions that regulates energy balance. So far, no data exist on NUCB2/nesfatin-1 localization in human and murine chondrocytes. Here, we therefore investigated NUCB2/nesfatin-1 gene and protein expression in human and murine chondrocytes and the effect of nesfatin-1 on pro-inflammatory cytokines expression. Peptide localization was performed by laser confocal microscopy, NUCB2 mRNA expression was studied by RT-PCR and protein secretion was measured by XMap technology and Western blot analysis. First, we demonstrated cytoplasmic localization of NUCB2/nesfatin-1 peptide in both human and murine chondrocytes. We present evidence that both mRNA and protein expression of NUCB2 were increased during the differentiation of ATDC5 murine chondrocyte cell line. Furthermore, we demonstrated that nesfatin-1 induces IL-6 and MIP-1alpha mRNA expression and protein secretion in ATDC-5 cells challenged with IL-1, and also increases COX-2 mRNA expression in these cells. Finally, nesfatin-1 provoked a clear induction of pro-inflammatory agents, such as COX-2, IL-8, IL-6, and MIP-1alpha in human primary chondrocytes from OA patients.

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