P2X7 receptor induces microglia polarization to the M1 phenotype in cancer-induced bone pain rat models

被引：18

作者：

Wu, Ping ^{[1
]}

Zhou, Guohua ^{[2
]}

Wu, Xiaoqi ^{[2
]}

Lv, Run ^{[3
]}

Yao, Jiaqi ^{[1
]}

Wen, Qingping ^{[1
]}

机构：

[1] Dalian Med Univ, Affiliated Hosp 1, Dept Anesthesiol, 222 Zhongshan Rd, Dalian 116000, Peoples R China

[2] Dalian Med Univ, Anesthesiol Dept, Dalian, Peoples R China

[3] Hebei Med Univ, Hosp 1, Dept Anesthesiol, Shijiazhuang, Hebei, Peoples R China

来源：

MOLECULAR PAIN | 2022年 / 18卷

关键词：

Cancer-induced bone pain; microglia polarization; BV2; NEUROPATHIC PAIN; SENSITIZATION; NEUROINFLAMMATION; HYPERSENSITIVITY; CONTRIBUTES; INVOLVEMENT; ACTIVATION; MECHANISMS; GLIA;

D O I：

10.1177/17448069211060962

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Background The transition from pro-inflammatory M1 phenotype to anti-inflammatory M2 phenotype presents a novel therapeutic strategy for chronic pain. Objective We investigated the role of microglia polarization in cancer-induced bone pain (CIBP), as well as the role of the P2X7 receptor in modulating M1 to M2 polarization. Methods Walker-256 breast cancer cells were administered into tibias of female rats to induce bone cancer-associated cancer. Results During bone cancer development, the P2X7 receptor and M1 microglia markers were upregulated. In contrast, inhibition of the P2X7 receptor by BBG, a blood-brain barrier-permeable P2X7R-specific antagonist, alleviated the pain and promoted microglia polarization toward the M2 phenotype, while suppressing the M1 phenotype in vivo and in vitro. Conclusion P2X7 receptor-mediated spinal microglia polarization is involved in alleviation of CIBP. Therefore, P2X7R is a potential option for CIBP treatment.

引用

页数：11

共 38 条

[1] Ethanol differentially modulates P2X4 and P2X7 receptor activity and function in BV2 microglial cells [J].

Asatryan, Liana ;

Ostrovskaya, Olga ;

Lieu, Dustin ;

Davies, Daryl L. .

NEUROPHARMACOLOGY, 2018, 128 :11-21

[2] P2X7 Receptor Activation Induces Reactive Oxygen Species Formation and Cell Death in Murine EOC13 Microglia [J].

Bartlett, Rachael ;

Yerbury, Justin J. ;

Sluyter, Ronald .

MEDIATORS OF INFLAMMATION, 2013, 2013

[3] P2X receptor channels in chronic pain pathways [J].

Bernier, Louis-Philippe ;

Ase, Ariel R. ;

Seguela, Philippe .

BRITISH JOURNAL OF PHARMACOLOGY, 2018, 175 (12) :2219-2230

[4] The Microglial ATP-Gated Ion Channel P2X7 As a CNS Drug Target [J].

Bhattacharya, Anindya ;

Biber, Knut .

GLIA, 2016, 64 (10) :1772-1787

[5] Suppression of KCNQ/ME (Kv7) potassium channels in the spinal cord contributes to the sensitization of dorsal horn WDR neurons and pain hypersensitivity in a rat model of bone cancer pain [J].

Cai, Jie ;

Fang, Dong ;

Liu, Xiao-Dan ;

Li, Song ;

Ren, Juan ;

Xing, Guo-Gang .

ONCOLOGY REPORTS, 2015, 33 (03) :1540-1550

[6] Disruption of the P2X7 purinoceptor gene abolishes chronic inflammatory and neuropathic pain [J].

Chessell, IP ;

Hatcher, JP ;

Bountra, C ;

Michel, AD ;

Hughes, JP ;

Green, P ;

Egerton, J ;

Murfin, M ;

Richardson, J ;

Peck, WL ;

Grahames, CBA ;

Casula, MA ;

Yiangou, Y ;

Birch, R ;

Anand, P ;

Buell, GN .

PAIN, 2005, 114 (03) :386-396

[7] Animal models of bone cancer pain: Systematic review and meta-analyses [J].

Currie, Gillian L. ;

Delaney, Ada ;

Bennett, Michael I. ;

Dickenson, Anthony H. ;

Egan, Kieren J. ;

Vesterinen, Hanna M. ;

Sena, Emily S. ;

Macleod, Malcolm R. ;

Colvin, Lesley A. ;

Fallon, Marie T. .

PAIN, 2013, 154 (06) :917-926

[8] Pain and Nociception: Mechanisms of Cancer-Induced Bone Pain [J].

Falk, Sarah ;

Dickenson, Anthony H. .

JOURNAL OF CLINICAL ONCOLOGY, 2014, 32 (16) :1647-1654

[9] Spinal Injection of TNF-α-activated Astrocytes Produces Persistent Pain Symptom Mechanical Allodynia by Releasing Monocyte Chemoattractant Protein-1 [J].

Gao, Yong-Jing ;

Zhang, Ling ;

Ji, Ru-Rong .

GLIA, 2010, 58 (15) :1871-1880

[10] EVOKED PAIN BEHAVIOR AND SPINAL GLIA ACTIVATION IS DEPENDENT ON TUMOR NECROSIS FACTOR RECEPTOR 1 AND 2 IN A MOUSE MODEL OF BONE CANCER PAIN [J].

Geis, C. ;

Graulich, M. ;

Wissmann, A. ;

Hagenacker, T. ;

Thomale, J. ;

Sommer, C. ;

Schaefers, M. .

NEUROSCIENCE, 2010, 169 (01) :463-474

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