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dc.contributor.authorBravo Caparrós, Inmaculada
dc.contributor.authorRuiz Cantero, María del Carmen 
dc.contributor.authorPerazzoli, Gloria
dc.contributor.authorCronin, SFJ
dc.contributor.authorVela, José Miguel
dc.contributor.authorHamed, MF
dc.contributor.authorPenninger, JM
dc.contributor.authorBaeyens Cabrera, José Manuel 
dc.contributor.authorCobos del Moral, Enrique José 
dc.contributor.authorNieto López, Francisco Rafael 
dc.date.accessioned2021-03-11T08:12:48Z
dc.date.available2021-03-11T08:12:48Z
dc.date.issued2020-04
dc.identifier.citationBravo-Caparrós I, Ruiz-Cantero MC, Perazzoli G, Cronin SJF, Vela JM, Hamed MF, Penninger JM, Baeyens JM, Cobos EJ, Nieto FR. Sigma-1 receptors control neuropathic pain and macrophage infiltration into the dorsal root ganglion after peripheral nerve injury. FASEB J. 2020 Apr;34(4):5951-5966.es_ES
dc.identifier.urihttp://hdl.handle.net/10481/67088
dc.description.abstractNeuron-immune interaction in the dorsal root ganglia (DRG) plays a pivotal role in the neuropathic pain development after nerve injury. Sigma-1 receptor (Sig-1R) is expressed by DRG neurons but its role in neuropathic pain is not fully understood. We investigated the effect of peripheral Sig-1R on neuroinflammation in the DRG after spared (sciatic) nerve injury (SNI) in mice. Nerve injury induced a decrease in NeuN staining along with the nuclear eccentricity and ATF3 expression in the injured DRG. Sig-1R was present in all DRG neurons examined, and after SNI this receptor translocated to the periphery of the soma and the vicinity of the nucleus, especially in injured ATF3 + neurons. In WT mice, injured DRG produced the chemokine CCL2, and this was followed by massive infiltration of macrophages/monocytes, which clustered mainly around sensory neurons with translocated Sig-1R, accompanied by robust IL-6 increase and mechanical allodynia. In contrast, Sig-1R knockout (Sig-1R-KO) mice showed reduced levels of CCL2, decreased macrophage/monocyte infiltration into DRG, and less IL-6 and neuropathic mechanical allodynia after SNI. Our findings point to an important role of peripheral Sig-1R in sensory neuron-macrophage/monocyte communication in the DRG after peripheral nerve injury; thus, these receptors may contribute to the neuropathic pain phenotypees_ES
dc.description.sponsorshipNeurofarmacología del dolor de la Universidad de Granada (CTS-109)es_ES
dc.description.sponsorshipFPU grants from the Spanish Ministry of Education, Culture and Sports.es_ES
dc.description.sponsorshipSpanish Ministry of Economy and Competitiveness (MINECO, grant SAF2016-80540-R)es_ES
dc.description.sponsorshipthe Junta de Andalucía (grant CTS 109)es_ES
dc.description.sponsorshipEsteve Pharmaceuticalses_ES
dc.description.sponsorshipEuropean Regional Development Fund (ERDF)es_ES
dc.language.isoenges_ES
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es/*
dc.subjectATF3es_ES
dc.subjectCCL2es_ES
dc.subjectIL-6es_ES
dc.subjectNeuroinflammationes_ES
dc.subjectSpared nerve injuryes_ES
dc.subjectSigma-1 receptores_ES
dc.subjectNeuropathic paines_ES
dc.titleSigma-1 receptors control neuropathic pain and macrophage infiltration into the dorsal root ganglion after peripheral nerve injuryes_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.projectIDMINECO, grant SAF2016-80540-Res_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES
dc.identifier.doi10.1096/fj.201901921R
dc.type.hasVersioninfo:eu-repo/semantics/submittedVersiones_ES


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Except where otherwise noted, this item's license is described as Atribución-NoComercial-SinDerivadas 3.0 España