Upregulation of LncRNA71132 in the spinal cord regulates hypersensitivity in a rat model of bone cancer pain

Ni, Huadong; Xu, Miao; Kuang, Jiao; Xu, Chengfei; He, Qiuli; Luo, Ge; Fu, Jie; Zhu, Jianjun; Ni, Chaobo; Zhao, Baoxia; Xu, Longsheng; Zhou, Qinghe; Yao, Ming

doi:10.1097/j.pain.0000000000002678

Cited by 11 publications

(11 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The microRNA profiling database analysis disclosed that 45 microRNAs were significantly changed between Sham and BCP groups from 569 candidates ( Figure 2(b) ). 32 We then assessed the miR-155-5p temporal expression pattern in the spinal cord. The qPCR analysis was done to examine the variances in miR-155-5p levels in Sham and BCP groups; the miR-155-5p levels were markedly increased on day 12 post-BCP surgery in comparison with those after Sham surgery in the rat’s dorsal horn ( Figure 2(c) , *** p < 0.001 vs. Sham group; n = 4, one-way ANOVA).…”

Section: Resultsmentioning

confidence: 99%

miR-155-5p in the spinal cord regulates hypersensitivity in a rat model of bone cancer pain

Liu

Wang

et al. 2022

Mol Pain

Self Cite

View full text Add to dashboard Cite

Background: Noncoding microRNAs have emerged as critical players of gene expression in the nervous system, where they contribute to regulating nervous disease. As stated in previous research, the miR-155-5p upregulation happens in the spinal cord at the nociceptive state. It was unclear if miR-155-5p is linked to bone cancer pain (BCP). Herein, we aimed at investigating the miR-155-5p functional regulatory function in BCP process and delineating the underlying mechanism. Methods: The miRNA-155-5p levels and cellular distribution were determined by RNA sequencing, fluorescent in situ hybridization (FISH), and quantitative real-time PCR (qPCR). Immunoblotting, qPCR, dual-luciferase reporter gene assays, immunofluorescence, recombinant overexpression adeno-associated virus, small interfering RNA, intraspinal administration, and behavioral tests were utilized for exploring the downstream signaling pathway. Results: The miR-155-5p high expression in spinal neurons contributes to BCP maintenance. The miR-155-5p blockage via the intrathecal injection of miR-155-5p antagomir alleviated the pain behavior; in contrast, upregulating miR-155-5p by agomir induced pain hypersensitivity. The miR-155-5p bounds directly to TCF4 mRNA’s 3′ UTR. BCP significantly reduced protein expression of TCF4 versus the Sham group. The miR-155-5p inhibition relieved the spinal TCF4 protein’s down-expression level, while miR-155-5p upregulation by miR-155-5p agomir intrathecal injection decreased TCF4 protein expression in naïve rats. Additionally, TCF4 overexpression in BCP rats could increase Kv1.1. Moreover, TCF4 knockdown inhibited Kv1.1 expression in BCP rats. Indeed, TCF4 and Kv1.1 were co-expressed in BCP spinal cord neurons. Conclusion: The study findings stated the miR-155-5p pivotal role in regulating BCP by directly targeting TCF4 in spinal neurons and suggested that miR-155 could be a promising target in treating BCP.

show abstract

Section: Resultsmentioning

confidence: 99%

miR-155-5p in the spinal cord regulates hypersensitivity in a rat model of bone cancer pain

Liu

Wang

et al. 2022

Mol Pain

Self Cite

View full text Add to dashboard Cite

show abstract

“…Referring to earlier studies ( Ni et al, 2022 ), rats were thoroughly sedated with pentobarbital (50 mg/kg, i. p.) and afterwards the spinal cord was incised in 2.5-cm length using a sterile and specifically constructed PE-10 tube (Comet Bio, China), which was introduced into the expanded, subarachnoid cavity of the lumbar region. The unfixed point of the PE-10 tube was introduced into the subcutaneous tissue of the back to provide medication.…”

Section: Methodsmentioning

confidence: 99%

“…Utilizing a multiphoton confocal microscope (Leica Microsystems, Wetzlar, Germany) photos were taken. In addition, referring to the previous references ( Shen et al, 2014 ; Xu et al, 2014 ; Ni et al, 2022 ), we performed the comparison of fluorescence intensity between different groups by averaging the fluorescence intensity for the same magnification, the same spinal cord size, and by selecting several regions that did not completely overlap.…”

Section: Methodsmentioning

confidence: 99%

Catalpol ameliorates CFA-induced inflammatory pain by targeting spinal cord and peripheral inflammation

Zhao

Fu²,

Ni³

et al. 2022

Front. Pharmacol.

Self Cite

View full text Add to dashboard Cite

Chronic, inflammatory pain is an international health concern that severely diminishes individuals’ quality of life. Catalpol is an iridoid glycoside derived from the roots of Rehmannia glutinosa that possesses anti-inflammatory, antioxidant, and neuroprotective properties for the treating multiple kinds of disorders. Nevertheless, catalpol’s impacts on inflammatory pain and its potential methods of action are still unclear. The purpose of this investigation is to determine the mechanism of catalpol to reduce the inflammatory pain behaviors in a rat model with complete Freund’s adjuvant (CFA). Catwalk, Von-Frey, and open field testing were performed for behavioral assessment. Western blot analysis and real-time quantitative PCR (RT-PCR) were employed to identify variations in molecular expression, while immunofluorescence was utilized to identify cellular localization. Catalpol effectively reduced CFA-induced mechanical allodynia and thermal hyperalgesia when injected intrathecally. Moreover, catalpol can regulate the HDAC4/PPAR-γ-signaling pathway in CFA rat spinal cord neurons. Meanwhile catalpol significantly decreased the expression of the NF-κB/NLRP3 inflammatory axis in the spinal cord of CFA rats. In addition, both in vivo and in vitro research revealed that catalpol treatment inhibited astrocyte activation and increase inflammatory factor expression. Interestingly, we also found that catalpol could alleviate peripheral pain by inhibiting tissue inflammation. Taken together, the findings declared that catalpol may inhibit inflammatory pain in CFA rats by targeting spinal cord and peripheral inflammation.

show abstract

“…Inhibition of GPR85 by miR143 alleviates mechanical pain sensitivity in rats. [ 41 ] GPR132 SNI Male/mice 9-HODE, 13-HODE Gαq Macrophages Knockout of GPR132 diminishes SNI-induced mechanical pain sensitivity and substantially diminishes the secretion of TNFα, IL-6, and VEGF. [ 42 ] CIPN DRG GPR132 participates in CIPN by activating TRPV1 via PKC.…”

Section: Ogpcrs and Painmentioning

confidence: 99%

“…In the context of bone cancer pain (BCP), GPR85 has been demonstrated to play a vital role. In a study by Ni et al, it was found that both mRNA and protein expression of GPR85 were significantly increased in the dorsal horn of the spinal cord in a rat model of BCP and were mainly expressed on neurons [ 41 ]. Further studies showed that injection of AAV- Gpr8 5-shRNA in the dorsal horn of the spinal cord reduced mechanical pain sensitivity in rats.…”

Section: Ogpcrs and Painmentioning

confidence: 99%

The role of orphan G protein-coupled receptors in pain

Xu,

Wang,

et al. 2024

Heliyon

Self Cite

View full text Add to dashboard Cite

Upregulation of LncRNA71132 in the spinal cord regulates hypersensitivity in a rat model of bone cancer pain

Abstract: Supplemental Digital Content is Available in the Text.LncRNA71132 works as a miRNA sponge in miR-143-5p–mediated posttranscriptional modulation of GPR85 expression in bone cancer pain.

Cited by 11 publications

References 63 publications

miR-155-5p in the spinal cord regulates hypersensitivity in a rat model of bone cancer pain

miR-155-5p in the spinal cord regulates hypersensitivity in a rat model of bone cancer pain

Catalpol ameliorates CFA-induced inflammatory pain by targeting spinal cord and peripheral inflammation

The role of orphan G protein-coupled receptors in pain

Contact Info

Product

Resources

About