期刊
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
卷 2022, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2022/8188404
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资金
- National Natural Science Foundation of China [82071397, 82071332]
- youth fund of National Natural Science Foundation of China [81801230]
- Chongqing Natural Science Foundation [cstc2019jcyj-msxmX0830]
- Excellent Scientific Research Talent's Fund of the First affiliated hospital of Chongqing Medical University
This study found that lncRNA-AK046375 enhances MT2 expression by sequestering miR-491-5p, ameliorating oxidative-induced cell injury, and promoting the recovery of motor, learning, and memory functions post-TBI.
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.
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