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MiR-137–3p rescue motoneuron death by targeting calpain-2
Abstract
Brachial plexus root avulsion (BPRA) is a type of injury that leads to motor function loss as a result of motoneurons (MNs) degeneration. Here we identified that the reduced expression of rat miR-137-3p in the ventral horn of spinal cord was associated with MNs death. However, the pathophysiological role of miR-137-3p in root avulsion remains poorly understood. We demonstrated that the calcium-activated neutral protease-2 (calpain-2) was a direct target gene of miR-137-3p with miR-137-3p binding to the 3'-untranslated region of calpain-2. Silencing of calpain-2 suppressed the expression of neuronal nitric oxide synthase (nNOS), a primary source of nitric oxide (NO). After avulsion 2 weeks, up-regulation of miR-137-3p in the spinal cord reduced calpain-2 levels and nNOS expression inside spinal MNs, resulting in an amelioration of the MNs death. These events provide new insight into the mechanism by which upregulation of miR-137-3p can impair MN survival in the BPRA.
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“and miR-137 downregulation agrees with calpain-2 and Casp-3 overexpression [21].”
From MicroRNA-138-5p Targets Pro-Apoptotic Factors and Favors Neural Cell Survival: Analysis in the Injured Spinal Cord (2022) · cites this paper as [21]
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Regulation of cellular senescence by microRNAs
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Metadata
- Authors
- Tang, Y., Fu, R., Ling, Z.-M., Liu, L.-L., Yu, G.-Y., Li, W., Fang, X.-Y., Zhu, Z., Wu, W.-T., & Zhou, L.-H.
- Venue
- Nitric Oxide
- Publisher
- Elsevier BV
- Published
- 2018-04
- Volume
- 74
- Pages
- 74-85
- ISSN
- 1089-8603
- Cited by
- 18
- References
- 56
- Language
- en
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- creativecommons.org/licenses/by-nc-nd/4.0/ (vor)
- Funders
- National Science Foundation Council of China (31471030)
- Guangdong Science Foundations (2015A030311014)
- Guangzhou science and technology (201510010208)
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