Abstract：
:The irrefutable change in the expression of brain-enriched microRNAs (miRNAs) following ischemic stroke has promoted the development of radical miRNA-based therapeutics encompassing neuroprotection and neuronal restoration. Our previous report on the systems-level prediction of miR-9 in post-stroke-induced neurogenesis served as a premise to experimentally uncover the functional role of miR-9 in post-ischemic neuronal survival and regeneration. The oxygen-glucose deprivation (OGD) in SH-SY5Y cells significantly reduced miR-9 expression, while miR-9 mimic transfection enhanced post-ischemic neuronal cell viability. The next major objective involved the execution of a drug repositioning strategy to augment miR-9 expression via structure-based screening of Food and Drug Administration (FDA)-approved drugs that bind to Histone Deacetylase 4 (HDAC4), a known miR-9 target. Glucosamine emerged as the top hit and its binding potential to HDAC4 was verified by Molecular Dynamics (MD) Simulation, Drug Affinity Responsive Target Stability (DARTS) assay, and MALDI-TOF MS. It was intriguing that the glucosamine treatment 1-h post-OGD was associated with the increased miR-9 level as well as enhanced neuronal viability. miR-9 mimic or post-OGD glucosamine treatment significantly increased the cellular proliferation (BrdU assay), while the neurite outgrowth assay displayed elongated neurites. The enhanced BCL2 and VEGF parallel with the reduced NFκB1, TNF-α, IL-1β, and iNOS mRNA levels in miR-9 mimic or glucosamine-treated cells further substantiated their post-ischemic neuroprotective and regenerative efficacy. Hence, this study unleashes a potential therapeutic approach that integrates neuronal survival and regeneration via small-molecule-based regulation of miR-9 favoring long-term recovery against ischemic stroke.
journal_name
Cell Mol Neurobioljournal_title
Cellular and molecular neurobiologyauthors
Nampoothiri SS,Rajanikant GKdoi
10.1007/s10571-018-0642-1subject
Has Abstractpub_date
2019-03-01 00:00:00pages
223-240issue
2eissn
0272-4340issn
1573-6830pii
10.1007/s10571-018-0642-1journal_volume
39pub_type
杂志文章abstract：:We previously reported that inhibition of Rho-kinase (ROCK) by hydroxyl fasudil improves cognitive deficit and neuronal damage in rats with chronic cerebral ischemia (Huang et al., Cell Mol Neurobiol 28:757-768, 2008). In this study, fasudil mesylate (FM) was investigated for its neuroprotective potential in rats with...
journal_title：Cellular and molecular neurobiology
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journal_title：Cellular and molecular neurobiology
pub_type： 杂志文章
doi：10.1023/a:1006984402291
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journal_title：Cellular and molecular neurobiology
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journal_title：Cellular and molecular neurobiology
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journal_title：Cellular and molecular neurobiology
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journal_title：Cellular and molecular neurobiology
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journal_title：Cellular and molecular neurobiology
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更新日期：2014-04-01 00:00:00
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journal_title：Cellular and molecular neurobiology
pub_type： 杂志文章
doi：10.1007/BF02151904
更新日期：1996-12-01 00:00:00
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journal_title：Cellular and molecular neurobiology
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更新日期：2008-08-01 00:00:00
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journal_title：Cellular and molecular neurobiology
pub_type： 杂志文章
doi：10.1007/s10571-014-0052-y
更新日期：2014-07-01 00:00:00
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journal_title：Cellular and molecular neurobiology
pub_type： 杂志文章,评审
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更新日期：2000-02-01 00:00:00
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journal_title：Cellular and molecular neurobiology
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更新日期：2000-08-01 00:00:00
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更新日期：2005-06-01 00:00:00
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journal_title：Cellular and molecular neurobiology
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更新日期：2018-10-01 00:00:00
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journal_title：Cellular and molecular neurobiology
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journal_title：Cellular and molecular neurobiology
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journal_title：Cellular and molecular neurobiology
pub_type： 杂志文章,评审
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更新日期：2019-01-01 00:00:00
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journal_title：Cellular and molecular neurobiology
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更新日期：2007-08-01 00:00:00
abstract：:Levels of cyclic nucleotides and ornithine decarboxylase (ODC) activity were examined following the application of various kinds of stimuli to superior cervical sympathetic ganglia (SCG), nodose ganglia, and vagus nerve fibers excised from the rat. The level of cyclic GMP in the SCG rose rapidly to about 4.5- to 7.5-f...
journal_title：Cellular and molecular neurobiology
pub_type： 杂志文章
doi：10.1007/BF00710944
更新日期：1984-03-01 00:00:00
