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Protective effect of DLX6-AS1 silencing against cerebral ischemia/reperfusion induced impairments.


ABSTRACT: In the present study, we investigated the role of lncRNA mus distal-less homeobox 6 antisense 1 (DLX6-AS1) during cerebral impairment induced by stroke. DLX6-AS1 levels were upregulated during ischemia/reperfusion (I/R) and downregulation of DLX6-AS1 reduced acute injury and ameliorated long-term neurological impairments induced by cerebral I/R in mice. Additionally, silencing of DLX6-AS1 significantly decreased the neuronal apoptosis in vivo and in vitro. Furthermore, inhibition of miRNA-149-3p led to enhance the apoptosis, which confirmed that DLX6-AS1 could sponge miR-149-3p. Finally, BOK was predicted to be the target of miR-149-3p using TargetScanVert software. And the silencing of DLX6-AS1 inhibited BOK expression both in vivo and in vitro, which was reversed by a miR-149-3p inhibitor. At meantime, BOK promoted OGD/R induced apoptosis in N2a cells. Therefore, this suggests that miR-149-3p sponging by DLX6-AS1 may lead to cerebral neuron I/R-induced impairments through upregulation of apoptotic BOK activity, which offers a new approach to the treatment of stroke impairment.

SUBMITTER: Hu X 

PROVIDER: S-EPMC7746362 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

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Protective effect of DLX6-AS1 silencing against cerebral ischemia/reperfusion induced impairments.

Hu Xiamin X   Xiang Zifei Z   Zhang Wei W   Yu Zhijun Z   Xin Xiaoming X   Zhang Rong R   Deng Youping Y   Yuan Qiong Q  

Aging 20201118 22


In the present study, we investigated the role of lncRNA mus <i>distal-less homeobox 6 antisense 1 (DLX6-AS1)</i> during cerebral impairment induced by stroke. DLX6-AS1 levels were upregulated during ischemia/reperfusion (I/R) and downregulation of DLX6-AS1 reduced acute injury and ameliorated long-term neurological impairments induced by cerebral I/R in mice. Additionally, silencing of DLX6-AS1 significantly decreased the neuronal apoptosis in vivo and in vitro. Furthermore, inhibition of miRNA  ...[more]

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