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Article: Spinal glial activation in a new rat model of bone cancer pain produced by prostate cancer cell inoculation of the tibia

TitleSpinal glial activation in a new rat model of bone cancer pain produced by prostate cancer cell inoculation of the tibia
Authors
Issue Date2005
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/pain
Citation
Pain, 2005, v. 118 n. 1-2, p. 125-136 How to Cite?
AbstractStudies suggest that astrocytes and microglia in the spinal cord are involved in the development of persistent pain induced by tissue inflammation and nerve injury. However, the role of glial cells in bone cancer pain is not well understood. The present study evaluated the spinal glial activation in a novel rat model of bone cancer pain produced by injecting AT-3.1 prostate cancer cells into the unilateral tibia of male Copenhagen rats. The structural damage to the tibia was monitored by radiological analysis. The thermal hyperalgesia, mechanical hyperalgesia and allodynia, and spontaneous flinch were measured. The results showed that: (1) inoculation of prostate cancer cells, but not the vehicle Hank's solution, induced progressive bone destruction at the proximal epiphysis of the tibia from day 7-20 post inoculation; (2) the inoculation also induced progressive thermal hyperalgesia, mechanical hyperalgesia, mechanical allodynia, and spontaneous flinches; (3) astrocytes and microglia were significantly activated in the spinal cord ipsilateral to the cancer leg, characterized by enhanced immunostaining of both glial fibrillary acidic protein (GFAP, astrocyte marker) and OX-42 (microglial marker); (4) IL-1β was up-regulated in the ipsilateral spinal cord, evidenced by an increase of IL-1β immunostained astrocytes. These results demonstrate that injection of AT-3.1 prostate cancer cells into the tibia produces progressive hyperalgesia and allodynia associated with the progression of tibia destruction, indicating the successful establishment of a novel male rat model of bone cancer pain. Further, bone cancer activates spinal glial cells, which may release IL-1β and other cytokines and contribute to hyperalgesia. © 2005 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/188577
ISSN
2015 Impact Factor: 5.557
2015 SCImago Journal Rankings: 3.007
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, RXen_US
dc.contributor.authorLiu, Ben_US
dc.contributor.authorWang, Len_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorQiao, JTen_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorLao, Len_US
dc.date.accessioned2013-09-03T04:10:24Z-
dc.date.available2013-09-03T04:10:24Z-
dc.date.issued2005en_US
dc.identifier.citationPain, 2005, v. 118 n. 1-2, p. 125-136en_US
dc.identifier.issn0304-3959en_US
dc.identifier.urihttp://hdl.handle.net/10722/188577-
dc.description.abstractStudies suggest that astrocytes and microglia in the spinal cord are involved in the development of persistent pain induced by tissue inflammation and nerve injury. However, the role of glial cells in bone cancer pain is not well understood. The present study evaluated the spinal glial activation in a novel rat model of bone cancer pain produced by injecting AT-3.1 prostate cancer cells into the unilateral tibia of male Copenhagen rats. The structural damage to the tibia was monitored by radiological analysis. The thermal hyperalgesia, mechanical hyperalgesia and allodynia, and spontaneous flinch were measured. The results showed that: (1) inoculation of prostate cancer cells, but not the vehicle Hank's solution, induced progressive bone destruction at the proximal epiphysis of the tibia from day 7-20 post inoculation; (2) the inoculation also induced progressive thermal hyperalgesia, mechanical hyperalgesia, mechanical allodynia, and spontaneous flinches; (3) astrocytes and microglia were significantly activated in the spinal cord ipsilateral to the cancer leg, characterized by enhanced immunostaining of both glial fibrillary acidic protein (GFAP, astrocyte marker) and OX-42 (microglial marker); (4) IL-1β was up-regulated in the ipsilateral spinal cord, evidenced by an increase of IL-1β immunostained astrocytes. These results demonstrate that injection of AT-3.1 prostate cancer cells into the tibia produces progressive hyperalgesia and allodynia associated with the progression of tibia destruction, indicating the successful establishment of a novel male rat model of bone cancer pain. Further, bone cancer activates spinal glial cells, which may release IL-1β and other cytokines and contribute to hyperalgesia. © 2005 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/painen_US
dc.relation.ispartofPainen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAstrocytes - Metabolismen_US
dc.subject.meshBone Neoplasms - Metabolism - Pathology - Physiopathologyen_US
dc.subject.meshCell Transplantation - Pathologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshGlial Fibrillary Acidic Protein - Metabolismen_US
dc.subject.meshHindlimb - Pathology - Physiopathologyen_US
dc.subject.meshHyperalgesia - Metabolism - Physiopathologyen_US
dc.subject.meshInterleukin-1 - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshNeoplasm Transplantation - Pathologyen_US
dc.subject.meshNeuroglia - Cytology - Metabolismen_US
dc.subject.meshPain - Metabolism - Physiopathologyen_US
dc.subject.meshProstate - Pathologyen_US
dc.subject.meshProstatic Neoplasms - Pathology - Secondaryen_US
dc.subject.meshRatsen_US
dc.subject.meshSpinal Cord - Cytology - Metabolismen_US
dc.titleSpinal glial activation in a new rat model of bone cancer pain produced by prostate cancer cell inoculation of the tibiaen_US
dc.typeArticleen_US
dc.identifier.emailLao, L: lxlao1@hku.hken_US
dc.identifier.authorityLao, L=rp01784en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.pain.2005.08.001en_US
dc.identifier.pmid16154703-
dc.identifier.scopuseid_2-s2.0-27644537034en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27644537034&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume118en_US
dc.identifier.issue1-2en_US
dc.identifier.spage125en_US
dc.identifier.epage136en_US
dc.identifier.isiWOS:000233281800017-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridZhang, RX=7404864527en_US
dc.identifier.scopusauthoridLiu, B=55720712900en_US
dc.identifier.scopusauthoridWang, L=9036448600en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridQiao, JT=7103301572en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US

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