96 188

Cited 0 times in

Orthopedic surgery-induced cognitive dysfunction is mediated by CX3CL1/R1 signaling

DC Field Value Language
dc.contributor.author구본녀-
dc.contributor.author김소연-
dc.contributor.author김은정-
dc.contributor.author김정민-
dc.date.accessioned2021-09-29T00:48:27Z-
dc.date.available2021-09-29T00:48:27Z-
dc.date.issued2021-04-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/184045-
dc.description.abstractBackground: Postoperative pain is a common phenomenon after surgery and is closely associated with the development of postoperative cognitive dysfunction (POCD). Persistent pain and systemic inflammation caused by surgery have been suggested as key factors for the development of POCD. Fractalkine (CX3CL1) and its receptor, the CX3C chemokine receptor 1 (CX3CR1), are known to play a key role in pain and inflammation signaling pathways. Recent studies have shown that the regulation of CX3CR1/L1 signaling influences the development of various diseases including neuronal diseases. We determined whether CX3CR1/L1 signaling is a putative therapeutic target for POCD in a mouse model. Methods: Adult (9-11 weeks) male mice were treated with neutralizing antibody to block CX3CR1/L1 signaling both before and after surgery. Inflammatory and behavioral responses including pain were assessed postoperatively. Also, CX3CR1 mRNA level was assessed. Hippocampal astrocyte activation, Mao B expression, and GABA expression were assessed at 2 days after surgery following neutralizing antibody administration. Results: The behavioral response indicated cognitive dysfunction and development of pain in the surgery group compared with the control group. Also, increased levels of pro-inflammatory cytokines and CX3CR1 mRNA were observed in the surgery group. In addition, increased levels of GABA and increased Mao B expression were observed in reactive astrocytes in the surgery group; these responses were attenuated by neutralizing antibody administration. Conclusions: Increased CX3CR1 after surgery is both necessary and sufficient to induce cognitive dysfunction. CX3CR1 could be an important target for therapeutic strategies to prevent the development of POCD.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherBioMed Central-
dc.relation.isPartOfJOURNAL OF NEUROINFLAMMATION-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleOrthopedic surgery-induced cognitive dysfunction is mediated by CX3CL1/R1 signaling-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Anesthesiology and Pain Medicine (마취통증의학교실)-
dc.contributor.googleauthorInja Cho-
dc.contributor.googleauthorJeong Min Kim-
dc.contributor.googleauthorEun Jung Kim-
dc.contributor.googleauthorSo Yeon Kim-
dc.contributor.googleauthorEun Hee Kam-
dc.contributor.googleauthorEunji Cheong-
dc.contributor.googleauthorMinah Suh-
dc.contributor.googleauthorBon-Nyeo Koo-
dc.identifier.doi10.1186/s12974-021-02150-x-
dc.contributor.localIdA00193-
dc.contributor.localIdA00616-
dc.contributor.localIdA00816-
dc.contributor.localIdA00884-
dc.relation.journalcodeJ01626-
dc.identifier.eissn1742-2094-
dc.identifier.pmid33858422-
dc.subject.keywordCX3C chemokine receptor 1-
dc.subject.keywordGABA-
dc.subject.keywordHippocampus-
dc.subject.keywordInflammation-
dc.subject.keywordPostoperative cognitive dysfunction-
dc.subject.keywordPostoperative pain-
dc.contributor.alternativeNameKu, Bon Nyo-
dc.contributor.affiliatedAuthor구본녀-
dc.contributor.affiliatedAuthor김소연-
dc.contributor.affiliatedAuthor김은정-
dc.contributor.affiliatedAuthor김정민-
dc.citation.volume18-
dc.citation.number1-
dc.citation.startPage94-
dc.identifier.bibliographicCitationJOURNAL OF NEUROINFLAMMATION, Vol.18(1) : 94, 2021-04-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anesthesiology and Pain Medicine (마취통증의학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.