English   español  
Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/101885
Compartir / Impacto:
Estadísticas
Add this article to your Mendeley library MendeleyBASE
Citado 14 veces en Web of Knowledge®  |  Pub MebCentral Ver citas en PubMed Central  |  Ver citas en Google académico
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar otros formatos: Exportar EndNote (RIS)Exportar EndNote (RIS)Exportar EndNote (RIS)
Título

Clinicopathological correlations of podoplanin (gp38) expression in rheumatoid synovium and its potential contribution to fibroblast platelet crosstalk

Autor del Rey, Manuel J.; Faré, Regina; Izquierdo, Elena; Usategui, Alicia; Rodríguez-Fernández, José Luis ; Suárez-Fueyo, Abel; Cañete, Juan D.; Pablos, José Luis
Fecha de publicación 16-jun-2014
EditorPublic Library of Science
Citación PLoS ONE 9 (6): e99607
ResumenIntroduction: Synovial fibroblasts (SF) undergo phenotypic changes in rheumatoid arthritis (RA) that contribute to inflammatory joint destruction. This study was undertaken to evaluate the clinical and functional significance of ectopic podoplanin (gp38) expression by RA SF. Methods: Expression of gp38 and its CLEC2 receptor was analyzed by immunohistochemistry in synovial arthroscopic biopsies from RA patients and normal and osteoarthritic controls. Correlation between gp38 expression and RA clinicopathological variables was analyzed. In patients rebiopsied after anti-TNF-a therapy, changes in gp38 expression were determined. Platelet-SF coculture and gp38 silencing in SF were used to analyze the functional contribution of gp38 to SF migratory and invasive properties, and to SF platelet crosstalk. Results: gp38 was abundantly but variably expressed in RA, and it was undetectable in normal synovial tissues. Among clinicopathologigal RA variables, significantly increased gp38 expression was only found in patients with lymphoid neogenesis (LN), and RF or ACPA autoantibodies. Cultured synovial but not dermal fibroblasts showed strong constitutive gp38 expression that was further induced by TNF-a. In RA patients, anti-TNF-a therapy significantly reduced synovial gp38 expression. In RA synovium, CLEC2 receptor expression was only observed in platelets. gp38 silencing in cultured SF did not modify their migratory and invasive properties but reduced the expression of IL-6 and IL-8 genes induced by SF-platelet interaction. Conclusions: In RA, synovial expression of gp38 is strongly associated to LN and it is reduced after anti-TNF-a therapy. Interaction between gp38 and CLEC2 platelet receptor is feasible in RA synovium in vivo and can specifically contribute ton gene expression by SF.
Descripción 9 p.-4 fig.-2 tab.
Versión del editorhttp://dx.doi.org/10.1371/journal.pone.0099607
URI http://hdl.handle.net/10261/101885
DOI10.1371/journal.pone.0099607
ISSN1932-6203
E-ISSN1932-6203
Aparece en las colecciones: (CIB) Artículos
Ficheros en este ítem:
Fichero Descripción Tamaño Formato  
PLOS_one 2014.pdf965,11 kBAdobe PDFVista previa
Visualizar/Abrir
Mostrar el registro completo
 



NOTA: Los ítems de Digital.CSIC están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.