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Front Cell Neurosci. 2019 Feb 20;13:50. doi: 10.3389/fncel.2019.00050. eCollection 2019.

Silencing of lncRNA PKIA-AS1 Attenuates Spinal Nerve Ligation-Induced Neuropathic Pain Through Epigenetic Downregulation of CDK6 Expression.

Hu JZ1,2, Rong ZJ1,2, Li M1,2, Li P1,2,3, Jiang LY1,2, Luo ZX1,2, Duan CY1,2, Cao Y1,2, Lu HB2,4.

Author information

1
Department of Spine Surgery, Xiangya Hospital, Central South University, Changsha, China.
2
Key Laboratory of Organ Injury, Aging and Regenerative Medicine of Hunan Province, Xiangya Hospital, Central South University, Changsha, China.
3
Department of Obstetrics, Xiangya Hospital, Central South University, Changsha, China.
4
Department of Sports Medicine, Xiangya Hospital, Central South University, Changsha, China.

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.

KEYWORDS:

CDK6; long non-coding RNA; neuroinflammation; neuropathic pain; spinal cord injury

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