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mettl, neurons, pubmed, fig, cell, article, neuronal, mice, google, scholar, rna, primary, cas, hippocampus, cycle, analysis, modification, mouse, knockdown, central, brain, reduced, disease, alzheimers, expression, control, data, ccnd, deficits, significantly, protein, treatment, cells, increased, mrna, cortical, death, hippocampal, representative, dysregulation, events, study, role, synaptic, loss, stress, caused, dna, methylation, immunoreactivity,

Topics {✒️}

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Questions {❓}

• How do pyramidal neurons commit to an unscheduled cell cycle after METTL3 knockdown that lead to their doomed fate?

Schema {🗺️}

WebPage:
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         headline:METTL3-dependent RNA m6A dysregulation contributes to neurodegeneration in Alzheimer’s disease through aberrant cell cycle events
         description:N6-methyladenosine (m6A) modification of RNA influences fundamental aspects of RNA metabolism and m6A dysregulation is implicated in various human diseases. In this study, we explored the potential role of RNA m6A modification in the pathogenesis of Alzheimer disease (AD). We investigated the m6A modification and the expression of m6A regulators in the brain tissues of AD patients and determined the impact and underlying mechanism of manipulated expression of m6A levels on AD-related deficits both in vitro and in vivo. We found decreased neuronal m6A levels along with significantly reduced expression of m6A methyltransferase like 3 (METTL3) in AD brains. Interestingly, reduced neuronal m6A modification in the hippocampus caused by METTL3 knockdown led to significant memory deficits, accompanied by extensive synaptic loss and neuronal death along with multiple AD-related cellular alterations including oxidative stress and aberrant cell cycle events in vivo. Inhibition of oxidative stress or cell cycle alleviated shMettl3-induced apoptotic activation and neuronal damage in primary neurons. Restored m6A modification by inhibiting its demethylation in vitro rescued abnormal cell cycle events, neuronal deficits and death induced by METTL3 knockdown. Soluble Aβ oligomers caused reduced METTL3 expression and METTL3 knockdown exacerbated while METTL3 overexpression rescued Aβ-induced synaptic PSD95 loss in vitro. Importantly, METTL3 overexpression rescued Aβ-induced synaptic damage and cognitive impairment in vivo. Collectively, these data suggested that METTL3 reduction-mediated m6A dysregulation likely contributes to neurodegeneration in AD which may be a therapeutic target for AD.
         datePublished:2021-09-30T00:00:00Z
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            RNA methylation
            METTL3
            Alzheimer’s disease
            Aberrant cell cycle events
            Apoptosis
            Neurosciences
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      headline:METTL3-dependent RNA m6A dysregulation contributes to neurodegeneration in Alzheimer’s disease through aberrant cell cycle events
      description:N6-methyladenosine (m6A) modification of RNA influences fundamental aspects of RNA metabolism and m6A dysregulation is implicated in various human diseases. In this study, we explored the potential role of RNA m6A modification in the pathogenesis of Alzheimer disease (AD). We investigated the m6A modification and the expression of m6A regulators in the brain tissues of AD patients and determined the impact and underlying mechanism of manipulated expression of m6A levels on AD-related deficits both in vitro and in vivo. We found decreased neuronal m6A levels along with significantly reduced expression of m6A methyltransferase like 3 (METTL3) in AD brains. Interestingly, reduced neuronal m6A modification in the hippocampus caused by METTL3 knockdown led to significant memory deficits, accompanied by extensive synaptic loss and neuronal death along with multiple AD-related cellular alterations including oxidative stress and aberrant cell cycle events in vivo. Inhibition of oxidative stress or cell cycle alleviated shMettl3-induced apoptotic activation and neuronal damage in primary neurons. Restored m6A modification by inhibiting its demethylation in vitro rescued abnormal cell cycle events, neuronal deficits and death induced by METTL3 knockdown. Soluble Aβ oligomers caused reduced METTL3 expression and METTL3 knockdown exacerbated while METTL3 overexpression rescued Aβ-induced synaptic PSD95 loss in vitro. Importantly, METTL3 overexpression rescued Aβ-induced synaptic damage and cognitive impairment in vivo. Collectively, these data suggested that METTL3 reduction-mediated m6A dysregulation likely contributes to neurodegeneration in AD which may be a therapeutic target for AD.
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      dateModified:2021-09-30T00:00:00Z
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         RNA m6A modification
         RNA methylation
         METTL3
         Alzheimer’s disease
         Aberrant cell cycle events
         Apoptosis
         Neurosciences
         Neurology
         Molecular Medicine
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            name:The University of Chicago
            address:
               name:Department of Chemistry, The University of Chicago, Chicago, USA
               type:PostalAddress
            type:Organization
      name:Chuan He
      affiliation:
            name:The University of Chicago
            address:
               name:Department of Chemistry, The University of Chicago, Chicago, USA
               type:PostalAddress
            type:Organization
            name:Howard Hughes Medical Institute, The University of Chicago
            address:
               name:Department of Biochemistry and Molecular Biology, Howard Hughes Medical Institute, The University of Chicago, Chicago, USA
               type:PostalAddress
            type:Organization
      name:Wenzhang Wang
      affiliation:
            name:Case Western Reserve University
            address:
               name:Department of Pathology, Case Western Reserve University, Cleveland, USA
               type:PostalAddress
            type:Organization
      name:James M. O’Donnell
      affiliation:
            name:University at Buffalo, the State University of New York
            address:
               name:Department of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, University at Buffalo, the State University of New York, Buffalo, USA
               type:PostalAddress
            type:Organization
      name:Beisha Tang
      affiliation:
            name:Central South University
            address:
               name:Department of Neurology, Xiangya Hospital, Central South University, Changsha, China
               type:PostalAddress
            type:Organization
      name:Xiongwei Zhu
      url:http://orcid.org/0000-0003-2092-6508
      affiliation:
            name:Case Western Reserve University
            address:
               name:Department of Pathology, Case Western Reserve University, Cleveland, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pathology, Case Western Reserve University, Cleveland, USA
      name:Department of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, University at Buffalo, the State University of New York, Buffalo, USA
      name:Department of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, University at Buffalo, the State University of New York, Buffalo, USA
      name:Department of Pathology, Case Western Reserve University, Cleveland, USA
      name:Department of Neurology, Xiangya Hospital, Central South University, Changsha, China
      name:Department of Pathology, Case Western Reserve University, Cleveland, USA
      name:Department of Pathology, Case Western Reserve University, Cleveland, USA
      name:Department of Chemistry, The University of Chicago, Chicago, USA
      name:Department of Chemistry, The University of Chicago, Chicago, USA
      name:Department of Chemistry, The University of Chicago, Chicago, USA
      name:Department of Biochemistry and Molecular Biology, Howard Hughes Medical Institute, The University of Chicago, Chicago, USA
      name:Department of Pathology, Case Western Reserve University, Cleveland, USA
      name:Department of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, University at Buffalo, the State University of New York, Buffalo, USA
      name:Department of Neurology, Xiangya Hospital, Central South University, Changsha, China
      name:Department of Pathology, Case Western Reserve University, Cleveland, USA

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