Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury
Our previous RNA sequencing study showed that the long non-coding RNA ischemia-related factor Vof-16 (lncRNA Vof-16) was upregulated after spinal cord injury, but its precise role in spinal cord injury remains unclear. Bioinformatics predictions have indicated that lncRNA Vof-16 may participate in t...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2022-01-01
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| Series: | Neural Regeneration Research |
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| Online Access: | http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=1;spage=217;epage=227;aulast=Zhang |
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| author | Xiao-Min Zhang Li-Ni Zeng Wan-Yong Yang Lu Ding Kang-Zhen Chen Wen-Jin Fu Si-Quan Zeng Yin-Ru Liang Gan-Hai Chen Hong-Fu Wu |
| author_facet | Xiao-Min Zhang Li-Ni Zeng Wan-Yong Yang Lu Ding Kang-Zhen Chen Wen-Jin Fu Si-Quan Zeng Yin-Ru Liang Gan-Hai Chen Hong-Fu Wu |
| author_sort | Xiao-Min Zhang |
| collection | DOAJ |
| description | Our previous RNA sequencing study showed that the long non-coding RNA ischemia-related factor Vof-16 (lncRNA Vof-16) was upregulated after spinal cord injury, but its precise role in spinal cord injury remains unclear. Bioinformatics predictions have indicated that lncRNA Vof-16 may participate in the pathophysiological processes of inflammation and apoptosis. PC12 cells were transfected with a pHBLV-U6-MCS-CMV-ZsGreen-PGK-PURO vector to express an lncRNA Vof-16 knockdown lentivirus and a pHLV-CMVIE-ZsGree-Puro vector to express an lncRNA Vof-16 overexpression lentivirus. The overexpression of lncRNA Vof-16 inhibited PC12 cell survival, proliferation, migration, and neurite extension, whereas lncRNA Vof-16 knockdown lentiviral vector resulted in the opposite effects in PC12 cells. Western blot assay results showed that the overexpression of lncRNA Vof-16 increased the protein expression levels of interleukin 6, tumor necrosis factor-α, and Caspase-3 and decreased Bcl-2 expression levels in PC12 cells. Furthermore, we established rat models of spinal cord injury using the complete transection at T10. Spinal cord injury model rats were injected with the lncRNA Vof-16 knockdown or overexpression lentiviral vectors immediately after injury. At 7 days after spinal cord injury, rats treated with lncRNA Vof-16 knockdown displayed increased neuronal survival and enhanced axonal extension. At 8 weeks after spinal cord injury, rats treated with the lncRNA Vof-16 knockdown lentiviral vector displayed improved neurological function in the hind limb. Notably, lncRNA Vof-16 knockdown injection increased Bcl-2 expression and decreased tumor necrosis factor-α and Caspase-3 expression in treated animals. Rats treated with the lncRNA Vof-16 overexpression lentiviral vector displayed opposite trends. These findings suggested that lncRNA Vof-16 is associated with the regulation of inflammation and apoptosis. The inhibition of lncRNA Vof-16 may be useful for promoting nerve regeneration and functional recovery after spinal cord injury. The experiments were approved by the Institutional Animal Care and Use Committee of Guangdong Medical University, China. |
| first_indexed | 2024-12-21T20:19:24Z |
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| id | doaj.art-2b8377478919498e8b694641b22b8eda |
| institution | Directory Open Access Journal |
| issn | 1673-5374 |
| language | English |
| last_indexed | 2024-12-21T20:19:24Z |
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| series | Neural Regeneration Research |
| spelling | doaj.art-2b8377478919498e8b694641b22b8eda2022-12-21T18:51:32ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742022-01-0117121722710.4103/1673-5374.314322Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injuryXiao-Min ZhangLi-Ni ZengWan-Yong YangLu DingKang-Zhen ChenWen-Jin FuSi-Quan ZengYin-Ru LiangGan-Hai ChenHong-Fu WuOur previous RNA sequencing study showed that the long non-coding RNA ischemia-related factor Vof-16 (lncRNA Vof-16) was upregulated after spinal cord injury, but its precise role in spinal cord injury remains unclear. Bioinformatics predictions have indicated that lncRNA Vof-16 may participate in the pathophysiological processes of inflammation and apoptosis. PC12 cells were transfected with a pHBLV-U6-MCS-CMV-ZsGreen-PGK-PURO vector to express an lncRNA Vof-16 knockdown lentivirus and a pHLV-CMVIE-ZsGree-Puro vector to express an lncRNA Vof-16 overexpression lentivirus. The overexpression of lncRNA Vof-16 inhibited PC12 cell survival, proliferation, migration, and neurite extension, whereas lncRNA Vof-16 knockdown lentiviral vector resulted in the opposite effects in PC12 cells. Western blot assay results showed that the overexpression of lncRNA Vof-16 increased the protein expression levels of interleukin 6, tumor necrosis factor-α, and Caspase-3 and decreased Bcl-2 expression levels in PC12 cells. Furthermore, we established rat models of spinal cord injury using the complete transection at T10. Spinal cord injury model rats were injected with the lncRNA Vof-16 knockdown or overexpression lentiviral vectors immediately after injury. At 7 days after spinal cord injury, rats treated with lncRNA Vof-16 knockdown displayed increased neuronal survival and enhanced axonal extension. At 8 weeks after spinal cord injury, rats treated with the lncRNA Vof-16 knockdown lentiviral vector displayed improved neurological function in the hind limb. Notably, lncRNA Vof-16 knockdown injection increased Bcl-2 expression and decreased tumor necrosis factor-α and Caspase-3 expression in treated animals. Rats treated with the lncRNA Vof-16 overexpression lentiviral vector displayed opposite trends. These findings suggested that lncRNA Vof-16 is associated with the regulation of inflammation and apoptosis. The inhibition of lncRNA Vof-16 may be useful for promoting nerve regeneration and functional recovery after spinal cord injury. The experiments were approved by the Institutional Animal Care and Use Committee of Guangdong Medical University, China.http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=1;spage=217;epage=227;aulast=Zhangapoptosis; functional recovery; inflammation; long non-coding rna ischemia related factor vof-16; nerve regeneration; nerve repair; neurite extension; neuronal survival; proliferation; spinal cord injury |
| spellingShingle | Xiao-Min Zhang Li-Ni Zeng Wan-Yong Yang Lu Ding Kang-Zhen Chen Wen-Jin Fu Si-Quan Zeng Yin-Ru Liang Gan-Hai Chen Hong-Fu Wu Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury Neural Regeneration Research apoptosis; functional recovery; inflammation; long non-coding rna ischemia related factor vof-16; nerve regeneration; nerve repair; neurite extension; neuronal survival; proliferation; spinal cord injury |
| title | Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury |
| title_full | Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury |
| title_fullStr | Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury |
| title_full_unstemmed | Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury |
| title_short | Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury |
| title_sort | inhibition of lncrna vof 16 expression promotes nerve regeneration and functional recovery after spinal cord injury |
| topic | apoptosis; functional recovery; inflammation; long non-coding rna ischemia related factor vof-16; nerve regeneration; nerve repair; neurite extension; neuronal survival; proliferation; spinal cord injury |
| url | http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=1;spage=217;epage=227;aulast=Zhang |
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