LncRNA BIRF Promotes Brain Ischemic Tolerance Induced By Cerebral Ischemic Preconditioning Through Upregulating GLT-1 via Sponging miR-330-5p.
LncRNA BIRF Promotes Brain Ischemic Tolerance Induced By Cerebral Ischemic Preconditioning Through Upregulating GLT-1 via Sponging miR-330-5p.
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LncRNA BIRF通过Sponging miR-330- 5 p上调GLT-1促进脑缺血预处理诱导的脑缺血耐受
DOI：
10.1007/s12035-022-02841-3
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发表时间：
2022-07
影响因子：
5.1
通讯作者：
Zhang, Min
中科院分区：
文献类型：
--
作者：
Li, Shichao;Zhang, Lingyan;Lin, Jiajie;Su, Achou;Liu, Xiyun;Zhang, Jingge;Xian, Xiaohui;Hu, Yuyan;Li, Wenbin;Sun, Shaoguang;Zhang, Min
长链非编码RNA（longnoncodingRNAs，lncRNAs）在多种疾病中起着重要的调控作用。然而，lncRNA在脑缺血预处理（CIPC）诱导的脑缺血耐受（BIT）中的作用尚不清楚。采用高通量测序技术分析缺血预处理后大鼠皮层星形胶质细胞lncRNA的表达谱。CCK-8法检测结果显示，一种新的lncRNA NONRATT009133.2与BIT高度相关，我们将其命名为脑缺血相关因子（BIRF）。通过生物信息学分析，我们预测BIRF、miR-330- 5 p和GLT-1（也称为Slc 1a 2）可能构成了一个诱导BIT的ceRNA调控网络。我们发现BIRF被CIPC上调，CIPC促进GLT-1表达和BIT诱导。BIRF可与miR-330- 5 p直接结合。此外，miR-330- 5 p直接靶向GLT-1，并且miR-330- 5 p在体外和体内抑制GLT-1表达和BIT诱导。此外，BIRF作为分子海绵与GLT-1 mRNA竞争性结合miR-330- 5 p，而miR-330- 5 p抑制剂逆转了BIRF siRNA对GLT-1表达和神经元活力的所有影响。总之，我们的结果证明了BIRF/miR-330- 5 p/GLT-1轴在CIPC诱导BIT中的重要作用。BIRF可能是一种潜在的有效治疗脑卒中损伤的策略。在线版本包含补充材料，可通过10.1007/s12035-022-02841-3获得。
Long noncoding RNAs (lncRNAs) play an important regulatory role in various diseases. However, the role of lncRNAs in brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIPC) is still unknown. The lncRNA profile of rat cortical astrocytes pretreated with ischemic preconditioning was analyzed by high-throughput sequencing. The results of Cell-Counting Kit-8 (CCK-8) assay showed that a novel lncRNA, NONRATT009133.2, which we referred to as brain ischemia–related factor (BIRF), was highly correlated with BIT. Through bioinformatics analysis, we predicted that BIRF, miR-330-5p, and GLT-1 (also named Slc1a2) might constitute a ceRNA regulatory network in the induction of BIT. We found that BIRF was upregulated by CIPC, which promoted GLT-1 expression and BIT induction. BIRF could directly bind to miR-330-5p. Furthermore, miR-330-5p directly targeted GLT-1, and miR-330-5p inhibited both GLT-1 expression and BIT induction in vitro and in vivo. Moreover, BIRF acts as a molecular sponge to competitively bind to miR-330-5p with GLT-1 mRNA, while the miR-330-5p inhibitor reversed all the effects of BIRF siRNA on GLT-1 expression and neuronal vitality. Taken together, our results demonstrate the important roles of the BIRF/miR-330-5p/GLT-1 axis in the induction of BIT by CIPC. BIRF may be a potentially effective therapeutic strategy against stroke injury. The online version contains supplementary material available at 10.1007/s12035-022-02841-3.
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影响因子：
8.3
作者：
Dykstra-Aiello C;Jickling GC;Ander BP;Shroff N;Zhan X;Liu D;Hull H;Orantia M;Stamova BS;Sharp FR
通讯作者：
Sharp FR
影响因子：
12.4
作者：
Vinciguerra A;Cepparulo P;Anzilotti S;Cuomo O;Valsecchi V;Amoroso S;Annunziato L;Pignataro G
通讯作者：
Pignataro G
影响因子：
8.3
作者：
PULSINELLI, WA;BRIERLEY, JB
通讯作者：
BRIERLEY, JB
影响因子：
30.8
作者：
Bhandari, Vinayak;Hoey, Christianne;Bristow, Robert G.
通讯作者：
Bristow, Robert G.
影响因子：
4.3
作者：
Li, En-yao;Zhao, Peng-ju;Wu, Hong
通讯作者：
Wu, Hong