000			nab a22 7a 4500
999			_c15980 _d15980
003			PC15980
005			20210625062816.0
008			200611b xxu||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_91881 _aRey Cerros, Manuel José del _eInstituto de Investigación i+12
100			_92671 _aFaré García, Regina _eInstituto de Investigación i+12
100			_91883 _aUsátegui Corral, Alicia _eInstituto de Investigación i+12
100			_92672 _aSuárez Fueyo, Abel _eInstituto de Investigación i+12
100			_91010 _aPablos Álvarez, José Luis _eReumatología
245	0	0	_aClinicopathological correlations of podoplanin (gp38) expression in rheumatoid synovium and its potential contribution to fibroblast platelet crosstalk. _h[artículo]
260			_bPloS one, _c2014
300			_a16;9(6):e99607.
500			_aFormato Vancouver: Del Rey MJ, Faré R, Izquierdo E, Usategui A, Rodríguez-Fernández JL, Suárez-Fueyo A et al. Clinicopathological correlations of podoplanin (gp38) expression in rheumatoid synovium and its potential contribution to fibroblast platelet crosstalk. PLoS One. 2014 Jun 16;9(6):e99607.
501			_aPMID: 24932813 PMC4059710
504			_aContiene 44 referencias
520			_aIntroduction: 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-α 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-α. In RA patients, anti-TNF-α 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-α therapy. Interaction between gp38 and CLEC2 platelet receptor is feasible in RA synovium in vivo and can specifically contribute to gene expression by SF.
710			_9625 _aInstituto de Investigación imas12
710			_9123 _aServicio de Reumatología
856			_uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059710/ _yAcceso libre
942			_2ddc _cART _n0