The BDNF-TrkB signaling pathway in the rostral anterior cingulate cortex is involved in the development of pain aversion in rats with bone cancer via NR2B and ERK-CREB signaling

Li, Jingjing; Wang, Xu; Wang, Hong; Wang, Ruiwei; Guo, Yanjing; Xu, Lichi; Zhang, Guang-Fen; Wu, Jiang‐Nan; Wang, Gongming

doi:10.1016/j.brainresbull.2022.04.001

Cited by 11 publications

(7 citation statements)

References 73 publications

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“…Previous studies have demonstrated that BDNF/TrkB signal can directly promote ERK cascade activation [ 35 , 36 , 37 , 38 ]. Therefore, we speculated that NCOR2 regulated the activation of the ERK pathway via BDNF/TrkB signal.…”

Section: Resultsmentioning

confidence: 99%

Knockdown of NCOR2 Inhibits Cell Proliferation via BDNF/TrkB/ERK in NF1-Derived MPNSTs

Chung

Aimaier

et al. 2022

Cancers

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(1) Background: malignant peripheral nerve sheath tumours (MPNSTs) are aggressive Schwann cell-derived sarcomas with dismal prognoses. Previous studies have shown that nuclear receptor corepressor 2 (NCOR2) plays a vital role in neurodevelopment and in various tumours. However, the impact of NCOR2 on the progression of MPNST remains unclear. (2) Methods: by GEO database, MPNST tissue microarray, and NF1-related tumour tissues and cell lines were used to explore NCOR2 expression level in the MPNSTs. The role and mechanism of NCOR2 in NF1-derived MPNSTs were explored by experiments in vivo and in vitro and by transcriptome high-throughput sequencing. (3) Results: NCOR2 expression is significantly elevated in NF1-derived MPNSTs and is associated with patient 10-year survival time. Knockdown of NCOR2 suppressed NF1-derived MPNST cell proliferation by blocking the cell cycle in the G0/G1 phase. Moreover, decreased NCOR2 expression could down-regulate MAPK signal activity through the BDNF/TrkB pathway. (4) Conclusions: our findings demonstrated that NCOR2 expression is significantly elevated in NF1-derived MPNSTs. NCOR2 knockdown can inhibit NF1-derived MPNST cell proliferation by weakened BDNF/TrkB/ERK signalling. Targeting NF1-derived MPNSTs with TrkB inhibitors, or in combination with ERK inhibitors, may be a novel therapeutic strategy for clinical trials.

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Section: Resultsmentioning

confidence: 99%

Knockdown of NCOR2 Inhibits Cell Proliferation via BDNF/TrkB/ERK in NF1-Derived MPNSTs

Chung

Aimaier

et al. 2022

Cancers

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“…It has been demonstrated that increased pain and pain aversion in bone pain rats is accompanied by the upregulation of brain-derived neurotrophic factor (BDNF) expression, and the phosphorylation of the ERK/CREB pathway (pERK/pCREB) is upregulated in response to increased pain and pain aversion (or the exogenous injection of BDNF). The decreased expression level of pERK/pCREB after blocking BDNF-TrkB signaling suggests that the ERK/CREB pathway is critical for BDNF-TrkB signaling-mediated pain and aversion pain, and this ERK/CREB pathway may induce pain in FD/MAS by mediating oxidative stress and neuroinflammatory processes [ 42 ].…”

Section: Effects Of the Erk/creb Pathway On Fd/mas Pain Mechanismsmentioning

confidence: 99%

Recent research advances in pain mechanisms in McCune–Albright syndrome thinking about the pain mechanism of FD/MAS

Wang,

Jiang

2024

J Orthop Surg Res

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Background The lack of effective understanding of the pain mechanism of McCune–Albright syndrome (MAS) has made the treatment of pain in this disease a difficult clinical challenge, and new therapeutic targets are urgently needed to address this dilemma. Objective This paper summarizes the novel mechanisms, targets, and treatments that may produce pain in MAS and fibrous dysplasia (polyfibrous dysplasia, or FD). Methods We conducted a systematic search in the PubMed database, Web of Science, China Knowledge Network (CNKI) with the following keywords: “McCune–Albright syndrome (MAS); polyfibrous dysplasia (FD); bone pain; bone remodeling; G protein coupled receptors; GDNF family receptors; purinergic receptors and glycogen synthase kinase”, as well as other keywords were systematically searched. Papers published between January 2018 and May 2023 were selected for finding. Initial screening was performed by reading the titles and abstracts, and available literature was screened against the inclusion and exclusion criteria. Results In this review, we systematically analyzed the cutting-edge advances in this disease, synthesized the findings, and discussed the differences. With regard to the complete mechanistic understanding of the pain condition in FD/MAS, in particular, we collated new findings on new pathways, neurotrophic factor receptors, purinergic receptors, interferon-stimulating factors, potassium channels, protein kinases, and corresponding hormonal modulation and their respective strengths and weaknesses. Conclusion This paper focuses on basic research to explore FD/MAS pain mechanisms. New nonneuronal and molecular mechanisms, mechanically loaded responsive neurons, and new targets for potential clinical interventions are future research directions, and a large number of animal experiments, tissue engineering techniques, and clinical trials are still needed to verify the effectiveness of the targets in the future.

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“…Subsequent pharmacological studies using NMDA GluN2B selective antagonists further confirmed that inhibition of ACC NMDA receptor GluN2B produced significant analgesic effects in animal models of chronic pain. 3 , 26 …”

Section: Glun2b and Chronic Painmentioning

confidence: 99%

Long-term plasticity of NMDA GluN2B (NR2B) receptor in anterior cingulate cortical synapses

Zhuo

2024

Mol Pain

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The anterior cingulate cortex (ACC) is a key cortical area for pain perception, emotional fear and anxiety. Cortical excitation is thought to be the major mechanism for chronic pain and its related emotional disorders such as anxiety and depression. GluN2B (or called NR2B) containing NMDA receptors play critical roles for such excitation. Not only does the activation of GluN2B contributes to the induction of the postsynaptic form of LTP (post-LTP), long-term upregulation of GluN2B subunits through tyrosine phosphorylation were also detected after peripheral injury. In addition, it has been reported that presynaptic NMDA receptors may contribute to the modulation of the release of glutamate from presynaptic terminals in the ACC. It is believed that inhibiting subtypes of NMDA receptors and/or downstream signaling proteins may serve as a novel therapeutic mechanism for future treatment of chronic pain, anxiety, and depression.

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The BDNF-TrkB signaling pathway in the rostral anterior cingulate cortex is involved in the development of pain aversion in rats with bone cancer via NR2B and ERK-CREB signaling

Cited by 11 publications

References 73 publications

Knockdown of NCOR2 Inhibits Cell Proliferation via BDNF/TrkB/ERK in NF1-Derived MPNSTs

Knockdown of NCOR2 Inhibits Cell Proliferation via BDNF/TrkB/ERK in NF1-Derived MPNSTs

Recent research advances in pain mechanisms in McCune–Albright syndrome thinking about the pain mechanism of FD/MAS

Long-term plasticity of NMDA GluN2B (NR2B) receptor in anterior cingulate cortical synapses

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