scholarly journals Endoplasmic reticulum stress impairment in the spinal dorsal horn of a neuropathic pain model

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Enji Zhang ◽  
Min-Hee Yi ◽  
Nara Shin ◽  
Hyunjung Baek ◽  
Sena Kim ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Neuropathic Pain ◽  
Endoplasmic Reticulum Stress ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Pain Model ◽  
Spinal Dorsal ◽  
Neuropathic Pain Model

Tanshinone II A Affects Diabetic Peripheral Neuropathic Pain via Spinal Dorsal Horn Neuronal Circuitry by Modulating Endoplasmic Reticulum Stress Pathways

2019 ◽  
Vol 128 (01) ◽  
pp. 59-65 ◽  
Author(s):  
Dawei Kong ◽  
Zhuangli Guo ◽  
Wenqiang Yang ◽  
Qi Wang ◽  
Yanbing Yu ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Neuropathic Pain ◽  
Endoplasmic Reticulum Stress ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Diabetic Group ◽  
Peripheral Neuropathic Pain ◽  
Tanshinone Ii A ◽  
Neuronal Circuitry ◽  
Spinal Dorsal

AbstractDiabetic peripheral neuropathic pain (DPNP) is a common manifestation of diabetic peripheral neuropathy (DPN). Although the pathogenesis of DPNP remains unclear, the disinhibition of spinal dorsal horn neuronal circuitry mediated by endoplasmic reticulum stress (ERS) is an important mechanism underlying neuropathic pain (NP). Tanshinone II A is mainly used to treat cardiovascular diseases but has also been shown to relieve various types of neuralgia, including DPNP. This study investigated the effects of tanshinone II A in DPNP model rats. We divided animals into two groups: 1) the model (diabetic) group and 2) the tanshinone II A-treatment group. Our results demonstrated that diabetic rats exhibited a decrease in the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL), and that NMT is increased and TWL is prolonged in rats treated with tanshinone II A. Additionally, the levels of ERS-signaling pathway factors in the spinal dorsal horns of rats were lower in the tanshinone II A-treated group than in the diabetic group. Overall, our study demonstrated that the disinhibition of spinal dorsal horn neuronal circuitry mediated by endoplasmic reticulum stress underlies DPNP and is modulated by tanshinone II A treatment.

mTOR pathway is involved in ADP-evoked astrocyte activation and ATP release in the spinal dorsal horn in a rat neuropathic pain model

Neuroscience ◽  
2014 ◽  
Vol 275 ◽  
pp. 395-403 ◽  
Author(s):  
J. Cui ◽  
W. He ◽  
B. Yi ◽  
H. Zhao ◽  
K. Lu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Atp Release ◽  
Mtor Pathway ◽  
Astrocyte Activation ◽  
Pain Model ◽  
Spinal Dorsal ◽  
Neuropathic Pain Model

Suberoylanilide Hydroxamic Acid Triggers Autophagy by Influencing the mTOR Pathway in the Spinal Dorsal Horn in a Rat Neuropathic Pain Model

2018 ◽  
Vol 44 (2) ◽  
pp. 450-464 ◽  
Author(s):  
Xiang-Lan Feng ◽  
Hong-Bo Deng ◽  
Zheng-Gang Wang ◽  
Yun Wu ◽  
Jian-Juan Ke ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Horn ◽  
Hydroxamic Acid ◽  
Spinal Dorsal Horn ◽  
Mtor Pathway ◽  
Suberoylanilide Hydroxamic Acid ◽  
Pain Model ◽  
Spinal Dorsal ◽  
Neuropathic Pain Model

scholarly journals Dexmedetomidine Alleviated Endoplasmic Reticulum Stress via Inducing ER-phagy in the Spinal Cord of Neuropathic Pain Model

2020 ◽  
Vol 14 ◽  
Author(s):  
Yongda Liu ◽  
Shuang Wang ◽  
Zhibin Wang ◽  
Mengmeng Ding ◽  
Xingyue Li ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Endoplasmic Reticulum ◽  
Neuropathic Pain ◽  
Endoplasmic Reticulum Stress ◽  
Pain Model ◽  
Neuropathic Pain Model

scholarly journals Endoplasmic reticulum stress promoting caspase signaling pathway-dependent apoptosis contributes to bone cancer pain in the spinal dorsal horn

2019 ◽  
Vol 15 ◽  
pp. 174480691987615
Author(s):  
Qiuli He ◽  
Tingting Wang ◽  
Huadong Ni ◽  
Qianying Liu ◽  
Kang An ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Pain ◽  
Signaling Pathway ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Spinal Dorsal

scholarly journals Calcitonin gene-related peptide regulates spinal microglial activation through the histone H3 lysine 27 trimethylation via enhancer of zeste homolog-2 in rats with neuropathic pain

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Qi An ◽  
Chenyan Sun ◽  
Ruidi Li ◽  
Shuhui Chen ◽  
Xinpei Gu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Horn ◽  
Nerve Injury ◽  
Spinal Dorsal Horn ◽  
Microglial Activation ◽  
Microglial Cells ◽  
Gene Promoters ◽  
Spinal Dorsal ◽  
Related Peptide ◽  
Calcitonin Gene

Abstract Background Calcitonin gene-related peptide (CGRP) as a mediator of microglial activation at the transcriptional level may facilitate nociceptive signaling. Trimethylation of H3 lysine 27 (H3K27me3) by enhancer of zeste homolog 2 (EZH2) is an epigenetic mark that regulates inflammatory-related gene expression after peripheral nerve injury. In this study, we explored the relationship between CGRP and H3K27me3 in microglial activation after nerve injury, and elucidated the underlying mechanisms in the pathogenesis of chronic neuropathic pain. Methods Microglial cells (BV2) were treated with CGRP and differentially enrichments of H3K27me3 on gene promoters were examined using ChIP-seq. A chronic constriction injury (CCI) rat model was used to evaluate the role of CGRP on microglial activation and EZH2/H3K27me3 signaling in CCI-induced neuropathic pain. Results Overexpressions of EZH2 and H3K27me3 were confirmed in spinal microglia of CCI rats by immunofluorescence. CGRP treatment induced the increased of H3K27me3 expression in the spinal dorsal horn and cultured microglial cells (BV2) through EZH2. ChIP-seq data indicated that CGRP significantly altered H3K27me3 enrichments on gene promoters in microglia following CGRP treatment, including 173 gaining H3K27me3 and 75 losing this mark, which mostly enriched in regulation of cell growth, phagosome, and inflammation. qRT-PCR verified expressions of representative candidate genes (TRAF3IP2, BCL2L11, ITGAM, DAB2, NLRP12, WNT3, ADAM10) and real-time cell analysis (RTCA) verified microglial proliferation. Additionally, CGRP treatment and CCI increased expressions of ITGAM, ADAM10, MCP-1, and CX3CR1, key mediators of microglial activation in spinal dorsal horn and cultured microglial cells. Such increased effects induced by CCI were suppressed by CGRP antagonist and EZH2 inhibitor, which were concurrently associated with the attenuated mechanical and thermal hyperalgesia in CCI rats. Conclusion Our findings highly indicate that CGRP is implicated in the genesis of neuropathic pain through regulating microglial activation via EZH2-mediated H3K27me3 in the spinal dorsal horn.

Driving effect of BDNF in the spinal dorsal horn on neuropathic pain

2021 ◽  
pp. 135965
Author(s):  
Zhou Wu ◽  
Xie Zhiping ◽  
Li Chengcai ◽  
Zelong Xing ◽  
Xie Shenke ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Spinal Dorsal

scholarly journals Expression of granulocyte colony-stimulating factor 3 receptor in the spinal dorsal horn following spinal nerve ligation-induced neuropathic pain

2017 ◽  
Vol 16 (2) ◽  
pp. 2009-2015 ◽  
Author(s):  
Enji Zhang ◽  
Sunyeul Lee ◽  
Min-Hee Yi ◽  
Yongshan Nan ◽  
Yinshi Xu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Spinal Nerve ◽  
Spinal Nerve Ligation ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Spinal Dorsal ◽  
Stimulating Factor
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