Abstract
Neuropathic pain is caused by dysfunction or primary injury of the somatosensory nervous system. Long noncoding RNAs (lncRNAs) play important roles in the development of neuropathic pain. However, the effects of lncRNA colon cancer associated transcript-1 (CCAT1) in neuropathic pain have not been reported. The model of bilateral sciatic nerve chronic constriction injuries (bCCI) is regarded as long-lasting mechanical hypersensitivity and cold allodynia, which is the representative symptom in the human subjects suffering from the neuropathic pain. In this study, we found that CCAT1 expression was decreased in the spinal dorsal horn, dorsal root ganglion (DRG), hippocampus, and anterior cingulate cortex (ACC) of rats with bCCI. The rats of bCCI presented the cold allodynia after the 14th day of postoperation. We furtherly showed that lncRNA CCAT1 decreased miR-155 expression and enhanced Serum and glucocorticoid regulated protein kinase 3 (SGK3) expression in the NGF-differentiated PC12 cell. We found that miR-155 expression was increased in the spinal dorsal horn, DRG, hippocampus, and ACC of rats with bCCI injuries. However, SGK3 expression was downregulated in the spinal dorsal horn, DRG, hippocampus, and ACC of rats with bCCI injuries. Moreover, lncRNA CCAT1 overexpression could alleviate the pain thresholds and inhibited expression of SGK3 could rescue this effect. In conclusion, these results suggested the crucial roles of CCAT1 and SGK3 in the neuropathic pain.
Highlights
Neuropathic pain is one kind of indirect or direct pain caused by the dysfunction or primary injury of the somatosensory nervous system, and is considered as one of the most serious public health problems [1,2,3,4]
We found that cancer associated transcript-1 (CCAT1) expression was decreased in the spinal dorsal horn, dorsal root ganglion (DRG), hippocampus, and anterior cingulate cortex (ACC) of rats with bilateral sciatic nerve chronic constriction injuries (bCCI)
We found that miR-155 expression was increased in the spinal dorsal horn, DRG, hippocampus, and ACC of rats with bCCI injuries
Summary
Neuropathic pain is one kind of indirect or direct pain caused by the dysfunction or primary injury of the somatosensory nervous system, and is considered as one of the most serious public health problems [1,2,3,4]. The main causes are that the molecular mechanisms underlying the neuropathic pain development remain elusive [9,10,11]. It is important to study the molecular mechanisms of neuropathic pain development. Increasing studies have suggested that lncRNAs can server crucial roles in cell development, proliferation, differentiation, migration and invasion [16,17,18,19,20]. Recent evidences have demonstrated that lncRNAs are upregulated or downregulated in neuropathic pain models, which support the potential role of lncRNAs as a novel group of targets for the treatment of neuropathic pain [21,22,23]. LncRNA CCAT1 plays important roles in the proliferation, www.impactjournals.com/oncotarget migration and invasion. LncRNA CCAT1 overexpression could alleviate the pain thresholds partly through regulating miR-155/SGK3 expression
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
