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miR-142-3p is a Potential Therapeutic Target for Sensory Function Recovery of Spinal Cord Injury
Spinal cord injury (SCI), which is a leading cause of disability in modern society, commonly results from trauma. It has been reported that application of sciatic nerve conditioning injury plays a positive role in repairing the injury of the ascending spinal sensory pathway in laboratory animals. Be...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557393/ https://www.ncbi.nlm.nih.gov/pubmed/26318123 http://dx.doi.org/10.12659/MSM.894098 |
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author | Wang, Tianyi Yuan, Wenqi Liu, Yong Zhang, Yanjun Wang, Zhijie Chen, Xueming Feng, Shiqing Xiu, Yucai Li, Wenhua |
author_facet | Wang, Tianyi Yuan, Wenqi Liu, Yong Zhang, Yanjun Wang, Zhijie Chen, Xueming Feng, Shiqing Xiu, Yucai Li, Wenhua |
author_sort | Wang, Tianyi |
collection | PubMed |
description | Spinal cord injury (SCI), which is a leading cause of disability in modern society, commonly results from trauma. It has been reported that application of sciatic nerve conditioning injury plays a positive role in repairing the injury of the ascending spinal sensory pathway in laboratory animals. Because of the complexity of SCI and related ethics challenges, sciatic nerve conditioning injury cannot be applied in clinical therapy. Accordingly, it is extremely important to study its mechanism and develop replacement therapy. Based on empirical study and clinical trials, this article suggests that miR-142-3p is the key therapeutic target for repairing sensory function, based on the following evidence. Firstly, studies have reported that endogenous cAMP is the upstream regulator of 3 signal pathways that are partially involved in the mechanisms of sciatic nerve conditioning injury, promoting neurite growth. The regulated miR-142-3p can induce cAMP elevation via adenylyl cyclase 9 (AC9), which is abundant in dorsal root ganglia (DRG). Secondly, compared with gene expression regulation in the injured spinal cord, inhibition of microRNA (miRNA) in DRG is less likely to cause trauma and infection. Thirdly, evidence of miRNAs as biomarkers and therapeutic targets in many diseases has been reported. In this article we suggest, for the first time, imitating sciatic nerve conditioning injury, thereby enhancing central regeneration of primary sensory neurons via interfering with the congenerous upstream regulator AC9 of the 3 above-mentioned signal pathways. We hope to provide a new clinical treatment strategy for the recovery of sensory function in SCI patients. |
format | Online Article Text |
id | pubmed-4557393 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-45573932015-09-15 miR-142-3p is a Potential Therapeutic Target for Sensory Function Recovery of Spinal Cord Injury Wang, Tianyi Yuan, Wenqi Liu, Yong Zhang, Yanjun Wang, Zhijie Chen, Xueming Feng, Shiqing Xiu, Yucai Li, Wenhua Med Sci Monit Hypothesis Spinal cord injury (SCI), which is a leading cause of disability in modern society, commonly results from trauma. It has been reported that application of sciatic nerve conditioning injury plays a positive role in repairing the injury of the ascending spinal sensory pathway in laboratory animals. Because of the complexity of SCI and related ethics challenges, sciatic nerve conditioning injury cannot be applied in clinical therapy. Accordingly, it is extremely important to study its mechanism and develop replacement therapy. Based on empirical study and clinical trials, this article suggests that miR-142-3p is the key therapeutic target for repairing sensory function, based on the following evidence. Firstly, studies have reported that endogenous cAMP is the upstream regulator of 3 signal pathways that are partially involved in the mechanisms of sciatic nerve conditioning injury, promoting neurite growth. The regulated miR-142-3p can induce cAMP elevation via adenylyl cyclase 9 (AC9), which is abundant in dorsal root ganglia (DRG). Secondly, compared with gene expression regulation in the injured spinal cord, inhibition of microRNA (miRNA) in DRG is less likely to cause trauma and infection. Thirdly, evidence of miRNAs as biomarkers and therapeutic targets in many diseases has been reported. In this article we suggest, for the first time, imitating sciatic nerve conditioning injury, thereby enhancing central regeneration of primary sensory neurons via interfering with the congenerous upstream regulator AC9 of the 3 above-mentioned signal pathways. We hope to provide a new clinical treatment strategy for the recovery of sensory function in SCI patients. International Scientific Literature, Inc. 2015-08-28 /pmc/articles/PMC4557393/ /pubmed/26318123 http://dx.doi.org/10.12659/MSM.894098 Text en © Med Sci Monit, 2015 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License |
spellingShingle | Hypothesis Wang, Tianyi Yuan, Wenqi Liu, Yong Zhang, Yanjun Wang, Zhijie Chen, Xueming Feng, Shiqing Xiu, Yucai Li, Wenhua miR-142-3p is a Potential Therapeutic Target for Sensory Function Recovery of Spinal Cord Injury |
title | miR-142-3p is a Potential Therapeutic Target for Sensory Function Recovery of Spinal Cord Injury |
title_full | miR-142-3p is a Potential Therapeutic Target for Sensory Function Recovery of Spinal Cord Injury |
title_fullStr | miR-142-3p is a Potential Therapeutic Target for Sensory Function Recovery of Spinal Cord Injury |
title_full_unstemmed | miR-142-3p is a Potential Therapeutic Target for Sensory Function Recovery of Spinal Cord Injury |
title_short | miR-142-3p is a Potential Therapeutic Target for Sensory Function Recovery of Spinal Cord Injury |
title_sort | mir-142-3p is a potential therapeutic target for sensory function recovery of spinal cord injury |
topic | Hypothesis |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557393/ https://www.ncbi.nlm.nih.gov/pubmed/26318123 http://dx.doi.org/10.12659/MSM.894098 |
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