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Article: Adiponectin Regulates Thermal Nociception In A Mouse Model Of Neuropathic Pain

TitleAdiponectin Regulates Thermal Nociception In A Mouse Model Of Neuropathic Pain
Authors
Keywordsadiponectin
hyperalgesia
neuralgia
neuroinflammation
p38 mitogen-activated protein kinase
Issue Date2018
PublisherOxford University Press. The Journal's web site is located at http://bja.oxfordjournals.org/
Citation
British Journal of Anaesthesia, 2018, v. 120 n. 6, p. 1356-1367 How to Cite?
AbstractBackground: Adiponectin, a cytokine secreted by adipocytes, plays an important role in regulating glucose and lipid metabolism. However, the role of adiponectin in pain conditions is largely unknown. This study aimed to identify the role and mechanism of adiponectin in nociceptive sensitivity under physiological and pathological states utilising adiponectin knockout (KO) mice. Methods: Wild type (WT) and adiponectin KO mice were subjected to partial sciatic nerve ligation (pSNL) or sham operation. Pain-like behavioural tests, including thermal allodynia, hyperalgesia, and mechanical allodynia, were performed before and after pSNL from Day 3–21. Dorsal root ganglions (DRGs), lumbar spinal segments at L3-5, and somatosensory cortex were collected for protein measurement via western blotting and immunofluorescence staining. Results: Compared with WT mice, KO mice had significantly lower (40–50%) paw withdrawal latency to innocuous and noxious stimuli before and after pSNL. In DRG neurones from KO mice, where adiponectin receptor (AdipoR) 2 is located, phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) and heat-sensitive transient receptor potential cation channel subfamily V member 1 (TRPV1) were significantly higher (by two- to three-fold) than from WT mice. In spinal microglia and somatosensory cortical neurones, where AdipoR1 is mainly located, p-p38 MAPK and TRPV1 were also higher (by two- to three-fold) in KO compared with WT mice, and altered signalling of these molecules was exacerbated (1.2- to 1.3-fold) by pSNL. Conclusions: Our results show that adiponectin regulates thermal nociceptive sensitivity by inhibiting activation of DRG neurones, spinal microglia, and somatosensory cortical neurones in physiological and neuropathic pain states. This study has relevance for patients with adiponectin disorders, such as obesity and diabetes.
DescriptionLink to Free access
Persistent Identifierhttp://hdl.handle.net/10722/279387
ISSN
2019 Impact Factor: 6.88
2015 SCImago Journal Rankings: 2.314

 

DC FieldValueLanguage
dc.contributor.authorSun, L-
dc.contributor.authorLi, H-
dc.contributor.authorTAI, LW-
dc.contributor.authorGU, P-
dc.contributor.authorCheung, CW-
dc.date.accessioned2019-11-01T07:16:20Z-
dc.date.available2019-11-01T07:16:20Z-
dc.date.issued2018-
dc.identifier.citationBritish Journal of Anaesthesia, 2018, v. 120 n. 6, p. 1356-1367-
dc.identifier.issn0007-0912-
dc.identifier.urihttp://hdl.handle.net/10722/279387-
dc.descriptionLink to Free access-
dc.description.abstractBackground: Adiponectin, a cytokine secreted by adipocytes, plays an important role in regulating glucose and lipid metabolism. However, the role of adiponectin in pain conditions is largely unknown. This study aimed to identify the role and mechanism of adiponectin in nociceptive sensitivity under physiological and pathological states utilising adiponectin knockout (KO) mice. Methods: Wild type (WT) and adiponectin KO mice were subjected to partial sciatic nerve ligation (pSNL) or sham operation. Pain-like behavioural tests, including thermal allodynia, hyperalgesia, and mechanical allodynia, were performed before and after pSNL from Day 3–21. Dorsal root ganglions (DRGs), lumbar spinal segments at L3-5, and somatosensory cortex were collected for protein measurement via western blotting and immunofluorescence staining. Results: Compared with WT mice, KO mice had significantly lower (40–50%) paw withdrawal latency to innocuous and noxious stimuli before and after pSNL. In DRG neurones from KO mice, where adiponectin receptor (AdipoR) 2 is located, phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) and heat-sensitive transient receptor potential cation channel subfamily V member 1 (TRPV1) were significantly higher (by two- to three-fold) than from WT mice. In spinal microglia and somatosensory cortical neurones, where AdipoR1 is mainly located, p-p38 MAPK and TRPV1 were also higher (by two- to three-fold) in KO compared with WT mice, and altered signalling of these molecules was exacerbated (1.2- to 1.3-fold) by pSNL. Conclusions: Our results show that adiponectin regulates thermal nociceptive sensitivity by inhibiting activation of DRG neurones, spinal microglia, and somatosensory cortical neurones in physiological and neuropathic pain states. This study has relevance for patients with adiponectin disorders, such as obesity and diabetes.-
dc.languageeng-
dc.publisherOxford University Press. The Journal's web site is located at http://bja.oxfordjournals.org/-
dc.relation.ispartofBritish Journal of Anaesthesia-
dc.rightsPre-print: Journal Title] ©: [year] [owner as specified on the article] Published by Oxford University Press [on behalf of xxxxxx]. All rights reserved. Pre-print (Once an article is published, preprint notice should be amended to): This is an electronic version of an article published in [include the complete citation information for the final version of the Article as published in the print edition of the Journal.] Post-print: This is a pre-copy-editing, author-produced PDF of an article accepted for publication in [insert journal title] following peer review. The definitive publisher-authenticated version [insert complete citation information here] is available online at: xxxxxxx [insert URL that the author will receive upon publication here].-
dc.subjectadiponectin-
dc.subjecthyperalgesia-
dc.subjectneuralgia-
dc.subjectneuroinflammation-
dc.subjectp38 mitogen-activated protein kinase-
dc.titleAdiponectin Regulates Thermal Nociception In A Mouse Model Of Neuropathic Pain-
dc.typeArticle-
dc.identifier.emailCheung, CW: cheucw@hku.hk-
dc.identifier.authorityCheung, CW=rp00244-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bja.2018.01.016-
dc.identifier.pmid29793601-
dc.identifier.scopuseid_2-s2.0-85047250614-
dc.identifier.hkuros308628-
dc.identifier.volume120-
dc.identifier.issue6-
dc.identifier.spage1356-
dc.identifier.epage1367-
dc.publisher.placeUnited Kingdom-

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