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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.

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


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.


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

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