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Silencing of lncRNA PKIA-AS1 Attenuates Spinal Nerve Ligation-Induced Neuropathic Pain Through Epigenetic Downregulation of CDK6 Expression
- Source :
- Frontiers in Cellular Neuroscience, Frontiers in Cellular Neuroscience, Vol 13 (2019)
- Publication Year :
- 2018
-
Abstract
- Neuropathic pain (NP) is among the most intractable comorbidities of spinal cord injury. Dysregulation of non-coding RNAs has also been implicated in the development of neuropathic pain. Here, we identified a novel lncRNA, PKIA-AS1, by using lncRNA array analysis in spinal cord tissue of spinal nerve ligation (SNL) model rats, and investigated the role of PKIA-AS1 in SNL-mediated neuropathic pain. We observed that PKIA-AS1 was significantly upregulated in SNL model rats and that PKIA-AS1 knockdown attenuated neuropathic pain progression. Alternatively, overexpression of PKIA-AS1 was sufficient to induce neuropathic pain-like symptoms in uninjured rats. We also found that PKIA-AS1 mediated SNL-induced neuropathic pain by directly regulating the expression and function of CDK6, which is essential for the initiation and maintenance of neuroinflammation and neuropathic pain. Therefore, our study identifies PKIA-AS1 as a novel therapeutic target for neuroinflammation related neuropathic pain.
- Subjects :
- 0301 basic medicine
CDK6
Bioinformatics
lcsh:RC321-571
neuroinflammation
03 medical and health sciences
Cellular and Molecular Neuroscience
0302 clinical medicine
Downregulation and upregulation
medicine
Gene silencing
lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry
Spinal cord injury
Neuroinflammation
Original Research
neuropathic pain
Gene knockdown
long non-coding RNA
business.industry
Spinal cord
medicine.disease
Long non-coding RNA
spinal cord injury
030104 developmental biology
medicine.anatomical_structure
Neuropathic pain
business
030217 neurology & neurosurgery
Neuroscience
Subjects
Details
- ISSN :
- 16625102
- Volume :
- 13
- Database :
- OpenAIRE
- Journal :
- Frontiers in cellular neuroscience
- Accession number :
- edsair.doi.dedup.....205f4f1563d4b1559625e3850b7ca7c9