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Research Article
Yingjun Ouyang
Guangzhou First People's Hospital, School of Medicine, South China University of Technology
Corresponding Author
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Ischemic stroke (IS), caused by a permanent or transient local reduction in blood supply to the brain, is one of the most widespread causes of public health problems in modern society. Long non-coding RNA (LncRNA) has been reported to be related to angiogenesis following IS. In this study, we explored the effect and potential molecular mechanism of lncRNA HOTAIR in IS. Permanent middle cerebral artery occlusion (pMCAO) model and oxygen and glucose deprivation (OGD) model were established. HOTAIR was increased in vivo and in vitro models post-ischemic. HOTAIR knockdown promoted neurological function recovery, manifesting in decreased modified neurological severity score, cerebral infarcted area, apoptosis and inflammation, and improved balance ability, spatial learning and memory ability. Silencing HOTAIR also improved the viability of OGD-induced N2a cells, and attenuated apoptosis and inflammation. HOTAIR can compete with KLF6 to bind to miR-148a-3p. miR-148a-3p knockdown or KLF6 overexpression partially reversed the effect of sh-HOTAIR on OGD-induced N2a cells. HOTAIR suppressed the activation of STAT3 pathway via the miR-148a-3p/KLF6 axis. To summarize, this study demonstrated that lncRNA HOTAIR absorbed miR-148a-3p and up-regulate KLF6 expression through ceRNA mechanism, and inhibited STAT3 pathway, promoted apoptosis and inflammation, and aggravated neurological injury post-IS.
Keywords
Ischemic stroke, LncRNA HOTAIR, microRNA-148a-3p, KLF6, Neurological function recovery, STAT3 signaling pathway, Apoptosis, Inflammation
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No competing interests reported.
This is a list of supplementary files associated with this preprint. Click to download.
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CURRENT STATUS: Under Revision
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Posted 12 Mar, 2021
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Editorial decision: Major revision
On 20 Apr, 2021
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Received 18 Apr, 2021
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On 07 Apr, 2021
Reviews received
Received 29 Mar, 2021
Reviewers agreed
On 19 Mar, 2021
Reviewers invited
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Editor assigned
On 08 Mar, 2021
Editor invited
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On 05 Mar, 2021
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Subject Areas
Cellular & Molecular Neuroscience
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This preprint is under consideration at Scientific Reports. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Yingjun Ouyang
Guangzhou First People's Hospital, School of Medicine, South China University of Technology
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Revision
Version 1
Posted 12 Mar, 2021
No community comments so far
Editorial decision: Major revision
On 20 Apr, 2021
Reviews received
Received 18 Apr, 2021
Reviewers agreed
On 07 Apr, 2021
Reviews received
Received 29 Mar, 2021
Reviewers agreed
On 19 Mar, 2021
Reviewers invited
Invitations sent on 08 Mar, 2021
Editor assigned
On 08 Mar, 2021
Editor invited
On 05 Mar, 2021
Submission checks complete
On 05 Mar, 2021
First submitted
On 28 Feb, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cellular & Molecular Neuroscience
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Ischemic stroke (IS), caused by a permanent or transient local reduction in blood supply to the brain, is one of the most widespread causes of public health problems in modern society. Long non-coding RNA (LncRNA) has been reported to be related to angiogenesis following IS. In this study, we explored the effect and potential molecular mechanism of lncRNA HOTAIR in IS. Permanent middle cerebral artery occlusion (pMCAO) model and oxygen and glucose deprivation (OGD) model were established. HOTAIR was increased in vivo and in vitro models post-ischemic. HOTAIR knockdown promoted neurological function recovery, manifesting in decreased modified neurological severity score, cerebral infarcted area, apoptosis and inflammation, and improved balance ability, spatial learning and memory ability. Silencing HOTAIR also improved the viability of OGD-induced N2a cells, and attenuated apoptosis and inflammation. HOTAIR can compete with KLF6 to bind to miR-148a-3p. miR-148a-3p knockdown or KLF6 overexpression partially reversed the effect of sh-HOTAIR on OGD-induced N2a cells. HOTAIR suppressed the activation of STAT3 pathway via the miR-148a-3p/KLF6 axis. To summarize, this study demonstrated that lncRNA HOTAIR absorbed miR-148a-3p and up-regulate KLF6 expression through ceRNA mechanism, and inhibited STAT3 pathway, promoted apoptosis and inflammation, and aggravated neurological injury post-IS.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
No competing interests reported.
This is a list of supplementary files associated with this preprint. Click to download.
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