LncRNA MALAT1 is Neuroprotective in a Rat Model of Spinal Cord Ischemia-reperfusion Injury Through miR-204 Regulation

被引:54
作者
Qiao, Yong [1 ]
Peng, Changliang [1 ]
Li, Ji [1 ]
Wu, Dongjin [1 ]
Wang, Xiuwen [1 ]
机构
[1] Shandong Univ, Hosp 2, Dept Spinal Surg, 247 Beiyuan Rd, Jinan 250033, Shandong, Peoples R China
关键词
MALAT-1; miR-204; spinal cord; ischemia/reperfusion injury; oxygen; glucose deprivation; MICROVASCULAR ENDOTHELIAL-CELLS; INHIBITS APOPTOSIS; RNA; AUTOPHAGY; STROKE; CANCER; OXYGEN; DEATH;
D O I
10.2174/1567202615666180712153150
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: This study was to investigate the neuroprotective effect of long non-coding RNAs Metastasis associated lung adenocarcinoma transcript-1 (lncRNA MALAT-1) in Spinal Cord Ischemic/Reperfusion Injury (SCIRI). Methods: Quantitative real-time PCR (RT-qPCR) was used to examine the expressions of MALAT1, miR-204 and Bcl-2, while western blot was performed to examine Bcl-2. Besides, apoptosis was evaluated by the percentage of cell viability and apoptotic cells. Neurological evaluation was performed by measuring hindlimb locomotor function. Results: The expression of MALAT1 and Bcl-2 was decreased, while miRNA-204 (miR-204) was up-regulated in rats SCIRI model and neurocyte lines under hypoxic conditions. Oxygen, Glucose Deprivation (OGD) promoted apoptosis of neurocytes, downregulated MALAT1 and Bcl-2 and elevated miR-204 expression, however, overexpression of MALAT1 notably reversed this trend. Nevertheless, knockdown of MALAT1 increased cell apoptosis, decreased MALAT1 and Bcl-2 but upregulated miR-204. MALAT1 overexpression-induced anti-apoptosis and knockdown-induced pro-apoptosis were obviously reversed by synchronously overexpression and knockdown of miR-204, respectively. MALAT1-treated SCIRI rats exhibited lower Motor Deficit Index (MDI) scores, higher levels of MALAT1 and Bcl-2 expression and lower miR-204 expression. Conclusion: Our data suggested that MALAT1 exerted neuroprotective effect in a rat model of SCIRI by regulating miR-204.
引用
收藏
页码:211 / 219
页数:9
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