000			02794na a2200265 4500
999			_c353 _d353
003			PC353
005			20210625062753.0
008			130622s2013 xxx||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_aCaso, Javier Rubén _92439 _eInstituto de Investigación i+12
100			_aGarcía Bueno, Borja _91897 _eInstituto de Investigación i+12
100			_aHinojosa, Ara E _92627 _eInstituto de Investigación i+12
100			_aLeza, Juan Carlos _91995 _eInstituto de Investigación i+12
100			_aMadrigal, José LM _92628 _eInstituto de Investigación i+12
245	0	0	_aDual effects of noradrenaline on astroglial production of chemokines and pro-inflammatory mediators. _h[artículo]
260			_bJournal of neuroinflammation, _c2013
300			_a10:81.
500			_aFormato Vancouver: Hinojosa AE, Caso JR, García-Bueno B, Leza JC, Madrigal JL. Dual effects of noradrenaline on astroglial production of chemokines and pro-inflammatory mediators. J Neuroinflammation. 2013 Jul 9;10:81.
501			_aPMID: 23837880
504			_aContiene 65 referencias
520			_aNoradrenaline (NA) is known to limit neuroinflammation. However, the previously described induction by NA of a chemokine involved in the progression of immune/inflammatory processes, such as chemokine (C-C motif) ligand 2 (CCL2)/monocyte chemotactic protein-1 (MCP-1), apparently contradicts NA anti-inflammatory actions. In the current study we analyzed NA regulation of astroglial chemokine (C-X3-C motif) ligand 1 (CX3CL1), also known as fractalkine, another chemokine to which both neuroprotective and neurodegenerative actions have been attributed. In addition, NA effects on other chemokines and pro-inflammatory mediators were also analyzed.
710			_9625 _aInstituto de Investigación imas12
856			_uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708781/ _yAcceso libre
942			_n0 _2ddc _cART