Cited by 36MicroRNA in disease regulationSpinal Cord Injury ResearchNeurological Disease Mechanisms and Treatments

Overexpression of microRNA-21 protects spinal cords against transient ischemia

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He, Fang, Ren, Yixing, Shi, Enyi, Liu, Kun, Yan, Lihui, Jiang, Xiaojing·2016·The Journal of Thoracic and Cardiovascular Surgery

Abstract

Objective MicroRNA (miRNA) molecules are involved in the response of the central nervous system to ischemia and reperfusion. We sought to test the hypothesis that overexpression of miRNA-21 can induce neuroprotection on spinal cords against transient ischemia. Methods Overexpression of miRNA-21 in vivo was conducted by means of intrathecal injection of lentivirus vectors containing pre-miRNA-21. The vehicle or control lentivirus vectors were given to the control group and the control vector group, respectively. Five days later, spinal cord ischemia was accomplished in rats by crossclamping the descending aorta just distal to the left subclavian artery for 14 minutes. Hind-limb motor function was assessed during 48 hours after ischemia using the Motor Deficit Index, and histologic examination was performed. Expressions of caspase-3, Fas ligand (Faslg), programmed cell death 4 (PDCD4), and miRNA-21 in the spinal cord were evaluated by quantitative real-time polymerase chain reaction and western blot analysis. Results Transfection of pre-miRNA-21 significantly enhanced expression of miRNA-21 in the spinal cord (P < .01 vs the control group) and dramatically downregulated expressions of caspase-3, Faslg, and PDCD4 (P < .01 vs the control group). Compared with the control group, Motor Deficit Index scores at 6, 12, 24, and 48 hours after reperfusion were markedly lower in rats with overexpression of miRNA-21 (P < .01). Histologic examination showed that many more intact motor neurons were preserved in the lumbar spinal cord of rats with overexpression of miRNA-21 (P < .01 vs the control group). Conclusions Overexpression of miRNA-21 exerts neuroprotective effects on spinal cords against ischemia-reperfusion injury, possibly by inhibition of the proapoptotic proteins Faslg and PDCD4.

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Authors
He, F., Ren, Y., Shi, E., Liu, K., Yan, L., & Jiang, X.
Affiliations
  • Fourth Affiliated Hospital of China Medical University (CN)
  • First Hospital of China Medical University (CN)
Corresponding author
Jiang, Xiaojing
Venue
The Journal of Thoracic and Cardiovascular Surgery
Publisher
Elsevier BV
Published
2016-12
Volume
152
Issue
6
Pages
1602-1608
ISSN
0022-5223 (ISSN-L)
OpenAlex
W2518442543
Cited by
36
References
32
Citations by year
2026: 2 · 2025: 1 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 6 · 2020: 2 · 2019: 5 · 2018: 8 · 2017: 4 · 2016: 1
FWCI
2.51
Type
journal article
Language
en
Open access
Locations
  • Journal of Thoracic and Cardiovascular Surgery (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
miR-21, spinal cord ischemia, ischemia-reperfusion injury, neuroprotection, lentiviral overexpression, Fas ligand, PDCD4, caspase-3, apoptosis, motor neuron survival, hindlimb motor function, aortic cross-clamping
MeSH terms
Animals, Disease Models, Animal, Male, Transfection, Blotting, Western, Reperfusion Injury, Lentivirus, Rats, Wistar, Neuroprotective Agents, Spinal Cord Ischemia, MicroRNAs, Apoptosis Regulatory Proteins, Rats, Caspase 3, Fas Ligand Protein, Real-Time Polymerase Chain Reaction

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