ArticleBMC neuroscience2006
Reciprocal regulation of nuclear factor kappa B and its inhibitor ZAS3 after peripheral nerve injury.
Article in BMC neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Transcription Repressor Hes1 Contributes to Neuropathic Pain Development by Modifying CDK9/RNAPII-Dependent SpinalInternational journal of molecular sciences · 2019Article
- MiR-101 relates to chronic peripheral neuropathic pain through targeting KPNB1 and regulating NF-κB signaling.The Kaohsiung journal of medical sciences · 2019Article
- The proinflammatory protein HMGB1 is a substrate of transglutaminase-2 and forms high-molecular weight complexes with autoantigens.The Journal of biological chemistry · 2018Article
- Nuclear factor-kappa B regulates pain and COMT expression in a rodent model of inflammation.Brain, behavior, and immunity · 2015Article
- Spinal NF-κB and chemokine ligand 5 expression during spinal glial cell activation in a neuropathic pain model.PloS one · 2015Article
- Experimental study of vein subvolution combined with neural stem cells to repair sciatic neurologic defects in rats.International journal of clinical and experimental pathology · 2015Article
- Defining the nociceptor transcriptome.Frontiers in molecular neuroscience · 2014Article
- Propofol's effect on the sciatic nerve: Harmful or protective?Neural regeneration research · 2013Article
- Novel estrogen target gene ZAS3 is overexpressed in systemic lupus erythematosus.Molecular immunology · 2013Article
- Upregulation of cystathionine beta-synthetase expression by nuclear factor-kappa B activation contributes to visceral hypersensitivity in adult rats with neonatal maternal deprivation.Molecular pain · 2012Article
- Immune reactions and nerve repair in mice with sciatic nerve injury 14 days after intraperitoneal injection of Brazil.Neural regeneration research · 2012Article
- Article
- Characterization of NF-kB-mediated inhibition of catechol-O-methyltransferase.Molecular pain · 2009Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNF-kappaB binds to the kappaB motif to regulate transcription of genes involved in growth, immunity and inflammation, and plays a pivotal role in the production of pro-inflammatory cytokines after nerve injuries. The zinc finger protein ZAS3 also binds to the kappaB or similar motif. In addition to competition for common DNA sites, in vitro experiments have shown that ZAS3 can inhibit NF-kappaB via the association with TRAF2 to inhibit the nuclear translocation of NF-kappaB. However, the physiological significance of the ZAS3-mediated inhibition of NF-kappaB has not been demonstrated. The purpose of this study is to characterize ZAS3 proteins in nervous tissues and to use spinal nerve ligation, a neuropathic pain model, to demonstrate a functional relationship between ZAS3 and NF-kappaB.
resultsImmunohistochemical experiments show that ZAS3 is expressed in specific regions of the central and peripheral nervous system. Abundant ZAS3 expression is found in the trigeminal ganglion, hippocampal formation, dorsal root ganglia, and motoneurons. Low levels of ZAS3 expressions are also found in the cerebral cortex and in the grey matter of the spinal cord. In those nervous tissues, ZAS3 is expressed mainly in the cell bodies of neurons and astrocytes. Together with results of Western blot analyses, the data suggest that ZAS3 protein isoforms with differential cellular distribution are produced in a cell-specific manner. Further, neuropathic pain confirmed by persistent mechanical allodynia was manifested in rats seven days after L5 and L6 lumbar spinal nerve ligation. Changes in gene expression, including a decrease in ZAS3 and an increase in the p65 subunit of NF-kappaB were observed in dorsal root ganglion ipsilateral to the ligation when compared to the contralateral side.
conclusionZAS3 is expressed in nervous tissues involved in cognitive function and pain modulation. The down-regulation of ZAS3 after peripheral nerve injury may lead to activation of NF-kappaB, allowing Wallerian regeneration and induction of NF-kappaB-dependent gene expression, including pro-inflammatory cytokines. We propose that reciprocal changes in the expression of ZAS3 and NF-kappaB might generate neuropathic pain after peripheral nerve injury.
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