JAK-STAT3 pathway regulates spinal astrocyte proliferation and neuropathic pain maintenance in rats

Emerging evidence reveals that lncRNAs play important roles in various pathological processes, but precious little indicates their regulatory role in neuropathic pain.

Download Full-text

Neuronal-derived Ccl7 drives neuropathic pain by promoting astrocyte proliferation

Neuroreport ◽

10.1097/wnr.0000000000000625 ◽

2016 ◽

Vol 27 (11) ◽

pp. 849-857 ◽

Cited By ~ 9

Author(s):

Bin Chang Ke ◽

Xia Xiao Huang ◽

Yang Li ◽

Li Ya Li ◽

Qin Xue Xu ◽

...

Keyword(s):

Neuropathic Pain ◽

Astrocyte Proliferation

Download Full-text

IL-17 contributed to the neuropathic pain following peripheral nerve injury by promoting astrocyte proliferation and secretion of proinflammatory cytokines

Molecular Medicine Reports ◽

10.3892/mmr.2016.6018 ◽

2016 ◽

Vol 15 (1) ◽

pp. 89-96 ◽

Cited By ~ 21

Author(s):

Caixia Sun ◽

Jin Zhang ◽

Li Chen ◽

Tanghua Liu ◽

Gaobing Xu ◽

...

Keyword(s):

Neuropathic Pain ◽

Peripheral Nerve ◽

Nerve Injury ◽

Proinflammatory Cytokines ◽

Peripheral Nerve Injury ◽

Astrocyte Proliferation

Download Full-text

Retraction: Gm5820, an antisense RNA of FGF1, suppresses FGF1 expression at the posttranscriptional level to inactivate the ERK/STAT3 pathway and alleviates neuropathic pain in mice

RSC Advances ◽

10.1039/d1ra90034j ◽

2021 ◽

Vol 11 (9) ◽

pp. 5024-5024

Author(s):

Laura Fisher

Keyword(s):

Neuropathic Pain ◽

Antisense Rna ◽

Stat3 Pathway ◽

Posttranscriptional Level

Retraction of ‘Gm5820, an antisense RNA of FGF1, suppresses FGF1 expression at the posttranscriptional level to inactivate the ERK/STAT3 pathway and alleviates neuropathic pain in mice’ by Xin Zhang et al., RSC Adv., 2019, 9, 28364–28376, DOI: 10.1039/C9RA03791H.

Download Full-text

Inhibition of lncRNA DILC attenuates neuropathic pain via the SOCS3/JAK2/STAT3 pathway

Bioscience Reports ◽

10.1042/bsr20194486 ◽

2020 ◽

Vol 40 (6) ◽

Cited By ~ 3

Author(s):

Yujie Liu ◽

Lu Feng ◽

Shichao Ren ◽

Yingxiu Zhang ◽

Jing Xue

Keyword(s):

Spinal Cord ◽

Neuropathic Pain ◽

Underlying Mechanism ◽

Janus Kinase ◽

Pcr Analysis ◽

Cytokine Signaling ◽

Primary Microglia ◽

Down Regulation ◽

Stat3 Pathway ◽

Socs3 Expression

Abstract Long noncoding RNAs (lncRNAs) have been involved in the development of multiple pathological processes including neuropathic pain. The aim of the present study is to investigate the role of lncRNA down-regulated in liver cancer stem cells (DILC) in the progression of neuropathic pain and its underlying mechanism. Neuropathic pain rat model was established with the bilateral chronic constriction injury (bCCI) method. The results from quantitative PCR analysis in the spinal cord showed that DILC was significantly up-regulated in rats with bCCI compared with the sham group. DILC down-regulation mediated by intrathecal administration of DILC siRNA significantly increased the mechanical shrinkage threshold (MWT) and paw withdrawal threshold latency (PWTL), decreased the positive frequency for nerve sensitivity to cold and suppressed the expression of inflammatory genes in bCCI rats. Down-regulation of DILC induced suppressor of cytokine signaling (SOCS3) expression and inhibited the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) in spinal cord tissues. Western blotting showed that down-regulation of DILC by DILC siRNA transfection induced SOCS3 expression and inhibited the expression of p-Janus kinase 2 (p-JAK2) and p-STAT3 and their downstream genes in primary microglia. Furthermore, down-regulation of DILC increased the viability of primary microglia, suppressed apoptosis, and inhibited the production of interleukin (IL)-6 and IL-1β in microglia. In contrast, overexpression of DILC showed the opposite functions to those of DILC knockdown. In conclusion, silence of lncRNA DILC attenuates neuropathic pain via SOCS3-induced suppression of the JAK2/STAT3 pathway.

Download Full-text