Protein post-translational modifications after spinal cord injury

Zhu, Shuang; Yang, Bo; Li, Sijing; Ge, Tong; Tan, Jianye; Wu, Guofeng; Li, Lin; Chen, Guo-Li; Chen, Qian; Lin, Li

doi:10.4103/1673-5374.308068

Cited by 5 publications

(1 citation statement)

References 88 publications

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“…Peripheral nerve injury often results in neuropathic pain, where afferent nerves release multiple molecules, such as chemokines (CCL2, CCL21, and CXCL1), colony-stimulating factor 1, and matrix metallopeptidase 9, induce microglia plasma cell proliferation and activation, following which activated microglia release various bioactive substances that signal neuronal and nonneuronal cells to facilitate pain transmission, which is critical for pain hypersensitivity [11][12][13][14].…”

Section: Discussionmentioning

confidence: 99%

The temporal and spatial signature of microglial transcriptome in neuropathic pain

Liu

Dai

et al. 2023

NeuroReport

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Microglial activation following peripheral nerve injury is crucial for neuropathic pain (NP) development; however, studies on time-specific and spatial characteristics of microglial transcriptome are scarce. Firstly, we comparatively analysed microglial transcriptome of different brain regions and multiple timepoints after nerve injury by analysing the gene expression profile of GSE180627 and GSE117320. Then, we performed a mechanical pain hypersensitivity test on 12 rat neuropathic pain models using von Frey fibres at various timepoints after nerve injury. To further explore the key gene clusters closely related to the neuropathic pain phenotype, we conducted a weighted gene co-expression network analysis (WGCNA) on the GSE60670 gene expression profile. Lastly, we performed a single-cell sequencing analysis on GSE162807 for identifying microglia subpopulations. We found that the trend of microglia's transcriptome changes after nerve injury was that mRNA expression changes mainly occur early after injury, which is also consistent with phenotypic changes (NP progression). We also revealed that in addition to spatial specificity, microglia are also temporally specific in NP progression following nerve injury. The WGCNA findings revealed that the functional analysis of the key module genes emphasized the endoplasmic reticulum's (ER's) crucial role in NP. In our single-cell sequencing analysis, microglia were clustered into 18 cell subsets, of which we identified specific subsets of two timepoints (D3/D7) post-injury. Our study further revealed the temporal and spatial gene expression specificity of microglia in neuropathic pain. These results contribute to our comprehensive understanding of the pathogenic mechanism of microglia in neuropathic pain.

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Section: Discussionmentioning

confidence: 99%

The temporal and spatial signature of microglial transcriptome in neuropathic pain

Liu

Dai

et al. 2023

NeuroReport

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Injection of Cerium Oxide Nanoparticles to Treat Spinal Cord Injury in Rats

Behroozi

Rahimi

Hamblin

et al. 2022

Journal of Neuropathology &Amp; Experimental Neurology

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This study investigated the effects of local injection of cerium oxide nanoparticles (CeONPs) in a rat spinal cord injury (SCI) model. Thirty-six adult male Wistar rats were divided into 4 groups: controls (healthy animals), sham (laminectomy), SCI (laminectomy+SCI induction), and treatment (laminectomy+SCI induction+intrathecal injection of CeONPs immediately after injury). SCI was induced using an aneurysm clip at the T12-T13 vertebral region. Motor performance and pain threshold tests were performed weekly; H&E staining and measurement of cavity sizes were performed 6 weeks after injury. The expression of granulocyte colony-stimulating factor (GCSF), P44/42 MAPK, P-P44/42 MAPK, Tau, myelin-associated glycoprotein(MAG) was evaluated after 6 weeks by Western blot. The Basso, Beattie, and Bresnahan locomotor scoring scales improved in animals receiving CeONPs compared with SCI animals. The cavity sizes were less in the treatment group. GCSF expression was similar in the animals receiving CeONPs compared with the SCI group but the expression of ERK1/ERK2 and phospho-ERK was lower than in the SCI group. Expression levels of Tau and MAG were significantly increased in treated animals compared to the SCI group. These data indicate that the use of CeONPs may improve motor functional recovery in SCI.

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Inflammasomes, Inflammation and Neuropathic Pain

Sharan,

Pal,

Saha

et al. 2024

The NLRP3 Inflammasome: An Attentive Arbiter of Inflammatory Response

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Inflammasomes such as NOD-like receptor protein 1 (NLRP1), NLRP3, NLR family CARD domain-containing protein 4 (NLRC4) and absent in melanoma 2 (AIM2) are the primary mediators of inflammation and its associated neuropathic pain. These inflammasomes are activated leading to various autoimmune & metabolic disorders, cancer, and other inflammatory diseases. The activation of inflammasomes occurs due to molecular alterations like mitochondrial dysfunction, neuroinflammation, lysosomal damage, oxidative stress, sensitization, and disinhibition, which lead to proinflammatory pathways causing inflammasome-related neuropathic pain. Among these inflammasomes, NLRP3 has been widely studied and proven to be the key player in the development of neuropathy. In this chapter, we have summarized the role of inflammasome and how NLRP3 is involved in neuropathic pain. Therefore, based on the facts available, it has been suggested that focusing on inflammasome activity may be a cutting-edge and successful treatment approach for neuropathic pain.

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Protein post-translational modifications after spinal cord injury

Cited by 5 publications

References 88 publications

The temporal and spatial signature of microglial transcriptome in neuropathic pain

The temporal and spatial signature of microglial transcriptome in neuropathic pain

Injection of Cerium Oxide Nanoparticles to Treat Spinal Cord Injury in Rats

Inflammasomes, Inflammation and Neuropathic Pain

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