ArticleCytotechnology2021
Long non-coding RNA ZFAS1 exerts a protective role to alleviate oxygen and glucose deprivation-mediated injury in ischemic stroke cell model through targeting miR-186-5p/MCL1 axis.
Article in Cytotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Bone Marrow Mesenchymal Stem Cell-Derived Exosomal KLF4 Alleviated Ischemic Stroke Through Inhibiting N6-Methyladenosine Modification Level of Drp1 by Targeting lncRNA-ZFAS1.Molecular neurobiology · 2023Article
- The protective effects of lncRNA ZFAS1/miR-421-3p/MEF2C axis on cerebral ischemia-reperfusion injury.Cell cycle (Georgetown, Tex.) · 2022Article
- The role of blood lnc-ZFAS1 in acute ischemic stroke: correlation with neurological impairment, inflammation, and survival profiles.Journal of clinical laboratory analysis · 2022Article
- Pathophysiology of Ischemic Stroke: Noncoding RNA Role in Oxidative Stress.Oxidative medicine and cellular longevity · 2022Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, accumulating articles have revealed that long non-coding RNAs (lncRNAs) play crucial roles in ischemic stroke (IS). A previous study found that lncRNA zinc finger antisense 1 (ZFAS1) was down-regulated in IS patients compared with healthy controls. However, the precise function of ZFAS1 in IS and its associated mechanism remain unclear. Cell viability was assessed by cell counting kit-8 (CCK8) assay. Cell apoptosis was analyzed by flow cytometry. Western blot assay and quantitative real-time polymerase chain reaction (qRT-PCR) were conducted to measure protein and RNA expression. The interaction between microRNA-186-5p (miR-186-5p) and ZFAS1 or MCL1 apoptosis regulator, BCL2 family member (MCL1) was confirmed by dual-luciferase reporter assay, RNA-pull down assay and RNA immunoprecipitation (RIP) assay. IS cell model was established through exposing N2a cells to oxygen and glucose deprivation (OGD). OGD exposure restrained the viability and induced the apoptosis of N2a cells. OGD exposure down-regulated the expression of ZFAS1 and up-regulated the level of miR-186-5p in a time-dependent manner. ZFAS1 overexpression alleviated OGD-mediated injury in IS cell model. MiR-186-5p was identified as a direct target of ZFAS1, and OGD-induced injury in IS cell model was attenuated by the silence of miR-186-5p. MiR-186-5p interacted with the 3' untranslated region (3'UTR) of MCL1 messenger RNA (mRNA). ZFAS1 positively regulated MCL1 mRNA expression by sequestering miR-186-5p in N2a cells. ZFAS1 overexpression-mediated protective effects in IS cell model were partly overturned by the overexpression of miR-186-5p. MCL1 silencing partly counteracted the protective effects mediated by miR-186-5p silencing in IS cell model. In conclusion, ZFAS1 overexpression exerted a protective role in IS cell model to attenuate OGD-induced injury through targeting miR-186-5p/MCL1 axis. ZFAS1/miR-186-5p/MCL1 signaling might be a novel diagnostic marker and promising treatment target for IS patients. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10616-021-00481-4.
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