000 nab a22 7a 4500
999 _c16702
_d16702
003 PC16702
005 20211221125600.0
008 211221b xxu||||| |||| 00| 0 eng d
040 _cH12O
041 _aeng
100 _91010
_aPablos Álvarez, José Luis
_eReumatología
245 0 0 _aVIP modulates IL-22R1 expression and prevents the contribution of rheumatoid synovial fibroblasts to IL-22-mediated joint destruction.
_h[artículo]
260 _bJournal of molecular neuroscience: MN,
_c2014
300 _a52(1):10-7.
500 _aFormato Vancouver: Carrión M, Juarranz Y, Seoane IV, Martínez C, González Álvaro I, Pablos JL et al. VIP modulates IL-22R1 expression and prevents the contribution of rheumatoid synovial fibroblasts to IL-22-mediated joint destruction. J Mol Neurosci. 2014 Jan;52(1):10-7.
501 _aPMID: 24254222
504 _aContiene 41 referencias
520 _aRheumatoid arthritis (RA) and osteoarthritis are two rheumatic diseases whose progression is associated with a chronic synovitis. Fibroblast-like synoviocytes (FLS) have been shown to play a pivotal role in initiating and perpetuating inflammatory and destructive processes in the rheumatoid joint. Recently, the stimulating role of IL-22 has been reported on RA-FLS contribution to joint destruction by means of the increase of proliferation and matrix-metalloproteinase-1 (MMP-1) and alarmin S100A8/A9 production. Besides, mediators potentially present in inflamed joints have been shown to increase the expression of IL-22/IL-22R1 axis, amplifying the capacity of FLS to respond to IL-22 signalling. Since targeting cytokines that govern FLS activation would allow controlling their contribution to synovial inflammation, the present study was designed to analyze the potential immunoregulatory capacity of vasoactive intestinal peptide (VIP) to counterbalance IL-22 effects on FLS behavior. Our results showed that VIP is able to downregulate the augmented expression of IL-22 specific receptor in FLS subjected to a proinflammatory milieu. Moreover, this study revealed the ability of VIP to inhibit the IL-22 stimulatory effects on proliferation as well as on expression of both MMP-1 and alarmins in RA-FLS. The present findings reinforce the potential of this neuroimmunopeptide as a therapeutic agent in rheumatic diseases.
710 _9123
_aServicio de Reumatología
710 _9625
_aInstituto de Investigación imas12
856 _uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/1/pc16702.pdf
_ySolicitar documento
942 _2ddc
_cART
_n0