Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0423716 (Neuropathic pain)
 1,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropathic pain is a somatosensory disorder which is caused by disease or nerve injury that affects the nervous system. microRNAs (miRNAs) are proved to play crucial roles in the development of neuropathic pain. However, the role of miR-202 in neuropathic pain is still unknown. Sprague-Dawley rats were used for constructing the neuropathic pain model. The expression of miR-202 was determined by quantitative real-time polymerase chain reaction. Potential target gene for miR-202 was measured using bioinformatics methods and Western blot analysis. In this study, we used rats to establish a neuropathic pain model and measured the effect of miR-202 in neuropathic pain. We demonstrated that miR-202 expression was downregulated in the spinal dorsal horn of bilateral sciatic nerve chronic constriction injury (bCCI) rat. However, miR-202 expression was not changed in the dorsal root ganglion, hippocampus, and anterior cingulated cortex of bCCI rat. We identified that RAP1A was a direct target gene of miR-202 in the PC12 cell. RAP1A expression was upregulated in the spinal dorsal horn of bCCI rat. Overexpression of miR-202 could improve the pain threshold for bCCI rats in both hindpaws, indicating that miR-202 overexpression could lighten the pain threshold for model rats. Moreover, RAP1A overexpression increased the pain threshold effect of miR-202 overexpression treated bCCI rats, indicating that miR-202 could lighten the pain threshold through inhibiting RAP1A expression. These data suggested that miR-202 acted pivotal roles in the development of neuropathic pain partly through targeting RAP1A gene.
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PMID:miR-202 modulates the progression of neuropathic pain through targeting RAP1A. 3052 98

Neuropathic pain (NP) after spinal cord injury (SCI) leads to compromised physical and cognitive functions in a majority of patients. Aberrant miRNA expression plays vital roles in the pathogenesis of SCI. This study aims to investigate the effect of miR-331-3p in rats following SCI. Microarray assay was performed in SCI- and sham-operated rats to evaluate the expression of miR-331-3p. Assigned SCI rats were treated with miR-331-3p agomiR alone or miR-331-3p agomiR plus RAP1A-expressing lentivirus or control agomiR. Rat locomotor performance was evaluated by BBB locomotor rating scale. Neuronal tissue damage and apoptosis were detected by histological analyses and Western blot. Inflammation in spinal cord was determined by detection of the expression of inflammatory genes with qRT-PCR, and ELISA. Downstream expression of RAP1A was measured by Western blot. The results showed that SCI induced the downregulation of miR-331-3p in the spinal cord of SCI rats. Overexpression of miR-331-3p improved the locomotor performance, reduced tissue damage, neuronal apoptosis and inflammation in rat SCI model. Rap1a (Ras-related protein Rap-1A) was predicted as a downstream target for miR-331-3p, and upregulation of RAP1A impaired the beneficial effect of miR-331-3p post- SCI, which was shown as worse locomotor activity, more severe tissue damage, as well as promoting apoptosis and inflammation in SCI rats. Furthermore, miR-331-3p reduced the activation of RAP1A downstream genes via inhibiting RAP1A expression. These findings indicate a protective role of miR- 331-3p in the development of SCI via the modulation of RAP1A, and may help to develop novel therapy against SCI-induced complications.
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PMID:microRNA-331-3p attenuates neuropathic pain following spinal cord injury via targeting RAP1A. 3226 65