Involvement of CX3CR1 in bone cancer pain through the activation of microglia p38 MAPK pathway in the spinal cord

Hu, Jihua; Yang, Jianping; Liu, Lei; Li, Caifang; Wang, Lina; Ji, Fuhai; Cheng, Hao

doi:10.1016/j.brainres.2012.05.020

Cited by 60 publications

(40 citation statements)

References 39 publications

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“…A rat model of bone cancer pain was established as described previously (Hu et al, 2012b;Wang et al, 2011). In brief, under anesthesia with 4% Chloral Hydrate Solution (400 mg/kg, i.p.…”

Section: Bone Cancer Pain Modelmentioning

confidence: 99%

“…L4-5 spinal cords segments were post fixed in the same fixative for 6 h at 4 1C, and then placed in a 20% sucrose solution overnight at 4 1C. Immunofluorescence was performed on 6 μm thick L4-5 transverse spinal section sand processed as previously described (Hu et al, 2012b). Both cell slides and tissue sections were incubated with primary antibodies for rabbit anti-rat p-Akt (1:100) or mouse anti-rat OX-42 (1:100) overnight at 4 1C.…”

Section: Immunofluorescencementioning

confidence: 99%

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MCP-1 stimulates spinal microglia via PI3K/Akt pathway in bone cancer pain

Jin

Yang

et al. 2015

Brain Research

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“…A rat model of bone cancer pain was established as described previously (Hu et al, 2012b;Wang et al, 2011). In brief, under anesthesia with 4% Chloral Hydrate Solution (400 mg/kg, i.p.…”

Section: Bone Cancer Pain Modelmentioning

confidence: 99%

Section: Immunofluorescencementioning

confidence: 99%

MCP-1 stimulates spinal microglia via PI3K/Akt pathway in bone cancer pain

Jin

Yang

et al. 2015

Brain Research

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“…They were reported to contribute to the development and/or maintenance of bone cancer pain [18][19][20], neuropathic pain [21,22], and Rao Sun and Zhibin Zhao contributed equally to this work. postoperative pain [23][24][25].…”

Section: Introductionmentioning

confidence: 98%

Glucocorticoid-Potentiated Spinal Microglia Activation Contributes to Preoperative Anxiety-Induced Postoperative Hyperalgesia

et al. 2016

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Clinically, preoperative anxiety adversely affected postoperative hyperalgesia. As stress-induced glucocorticoids (GCs) were reported to sensitize the activation of microglia, the present study investigated whether and how GCs and microglia played in the process of preoperative anxiety-induced postoperative hyperalgesia. The study used an animal model that exposed rats to single prolonged stress (SPS) procedure to induce preoperative anxiety-like behaviors 24 h before the plantar incisional surgery. Behavioral testing revealed that preoperative SPS enhanced the mechanical allodynia induced by plantar incision. SPS was also found to induce elevated circulating corticosterone levels, potentiate the activation of spinal microglia, and increase the expression of spinal proinflammatory cytokines. Inhibition of microglia by pretreatment with minocycline attenuated the SPS-enhanced mechanical allodynia, and this was accompanied by decreased activation of spinal microglia and expression of proinflammatory cytokines. Another experiment was conducted by administering RU486, the GC receptor (GR) antagonist, to rats. The results showed that RU486 suppressed SPS-induced and SPS-potentiated proinflammatory activation of spinal microglia and revealed analgesic effects. Together, these data indicated that inhibition of stress-induced GR activation attenuated the preoperative anxiety-induced exacerbation of postoperative pain, and the suppression of spinal microglia activation may underlie this anti-hyperalgesia effect. Pending further studies, these findings suggested that GR and spinal microglia may play important roles in the development of preoperative anxiety-induced postoperative hyperalgesia and may serve as novel targets to prevent this phenomenon.

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“…Subsequently, this work demonstrated that the crosstalk between PI3K/Akt and Raf/MEK/ERK signaling pathway was the important mechanism underlying the contribution of CXCR3 activation to the development of BCP, which was proved by the results that the PI3K or MEK inhibitor could alleviate the activation of both Akt and ERK1/2 respectively. Their experiments provide new evidence to support that CXCR3 participates in central sensitization in BCP condition, like some other chemokines and their receptors (Hu et al, 2012a;Hu et al, 2012b;Liou et al, 2012;Yin et al, 2010). The exploration for the underlying mechanism of CXCR3 activation reveals the complexity of the BCP mechanism.…”

Section: Introductionmentioning

confidence: 91%