The lncRNA-AK046375 Upregulates Metallothionein-2 by Sequestering miR-491-5p to Relieve the Brain Oxidative Stress Burden after Traumatic Brain Injury
| Autor: | Wei Tang, Weina Chai, Donglin Du, Yongzhi Xia, Yifan Wu, Li Jiang, Chongjie Cheng, Zongduo Guo, Xiaochuan Sun, Zhijian Huang, Jianjun Zhong |
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| Jazyk: | angličtina |
| Rok vydání: | 2022 |
| Předmět: |
Neurons
Transcriptional Activation Aging Article Subject Brain Apoptosis Hydrogen Peroxide Cell Biology General Medicine Biochemistry Mice Inbred C57BL Mice MicroRNAs Oxidative Stress Neuroprotective Agents Blood-Brain Barrier Astrocytes Brain Injuries Traumatic Animals Metallothionein RNA Long Noncoding Cells Cultured |
| Zdroj: | Oxidative Medicine and Cellular Longevity. |
| ISSN: | 1942-0900 |
| DOI: | 10.1155/2022/8188404 |
| Popis: | We previously discovered that traumatic brain injury (TBI) induces significant perturbations in long noncoding RNA (lncRNA) levels in the mouse cerebral cortex, and lncRNA-AK046375 is one of the most significantly changed lncRNAs after TBI. lncRNA-AK046375 overexpression and knockdown models were successfully constructed both in vitro and in vivo. In cultured primary cortical neurons and astrocytes, lncRNA-AK046375 sequestered miR-491-5p, thereby enhancing the expression of metallothionein-2 (MT2), which ameliorated oxidative-induced cell injury. In addition, upregulated lncRNA-AK046375 promoted the recovery of motor, learning, and memory functions after TBI in C57BL/6 mice, and the underlying mechanism may be related to ameliorated apoptosis, inhibited oxidative stress, reduced brain edema, and relieved loss of tight junction proteins at the blood-brain barrier in the mouse brain. Therefore, we conclude that lncRNA-AK046375 enhances MT2 expression by sequestering miR-491-5p, ultimately strengthening antioxidant activity, which ameliorates neurological deficits post-TBI. |
| Databáze: | OpenAIRE |
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