We are analyzing https://link.springer.com/article/10.1007/s13577-017-0187-5.

Title:
MicroRNA-30e regulates neuroinflammation in MPTP model of Parkinson’s disease by targeting Nlrp3 | Human Cell
Description:
Accumulating evidences suggest that neuroinflammation is a pathological hallmark of Parkinson’s disease (PD), a neurodegenerative disorder characterized by loss of dopaminergic neurons in substantia nigra pars compacta (SNpc). MicroRNAs have been recently recognized as crucial regulators of inflammatory responses. Here, we found significant downregulation of microRNA-30e (miR-30e) in SNpc of MPTP-induced PD mice. Next, we employed miR-30e agomir to upregulate miR-30e expression in MPTP-treated mice. Our results showed that delivery of miR-30e agomir remarkably improved motor behavioral deficits and neuronal activity, and inhibited the loss of dopamine neurons. Moreover, the increased α-synuclein protein expression in SNpc of MPTP-PD mice was alleviated by the upregulation of miR-30e. Further, miR-30e agomir administration also attenuated the marked increase of inflammatory cytokines, such as TNF-α, COX-2, iNOS, and restored the decreased secretion of BDNF in SNpc. In addition, we demonstrated for the first time that miR-30e directly targeted to Nlrp3, thus suppressing Nlrp3 mRNA and protein expression. Finally, miR-30e upregulation significantly inhibited the activation of Nlrp3 inflammasome as evident from the decreased Nlrp3, Caspase-1 and ASC expressions and IL-18 and IL-1β secretions. Taken together, our study demonstrates that miR-30e ameliorates neuroinflammation in the MPTP model of PD by decreasing Nlrp3 inflammasome activity. These findings suggesting that miR30e may be a key inflammation-mediated molecule that could be a potential target for PD therapeutics.
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Keywords {🔍}

mire, nlrp, mice, expression, snpc, mptp, article, pubmed, google, scholar, agomir, disease, fig, cas, parkinsons, inflammasome, protein, treatment, showed, activity, neuroinflammation, neuronal, decreased, injection, test, saline, cell, mrna, αsyn, model, mptppd, cells, loss, mptpinduced, results, usa, group, dopaminergic, upregulation, significantly, days, effect, analysis, inflammatory, bdnf, caspase, ilβ, utr, neurons, increased,

Topics {✒️}

hrp-conjugated goat anti-rabbit siyuan chen & qi gu microrna-30e regulates neuroinflammation article download pdf mir-30e agomir-treated mice mir-30e upregulation attenuated mptp-induced α-syn expression tumor necrosis factor-alpha dopaminergic olfactory-striatal interplay inflammation-related neurodegenerative disorders employed mir-30e agomir mir-30e agomir protected mir-30e markedly attenuated transforming growth factor-alpha enzyme-linked immunosorbent assay mir-30e upregulation decreased mir-30e ameliorates neuroinflammation key inflammation-mediated molecule mir-30e directly binds nlrp3 inflammasome-mediated neuroinflammation effectively attenuate mptp-induced mir-30e agomir administration catechol-o-methyltransferase inhibitors upregulate mir-30e expression mir-30e directly targeted mir-30e agomir delivery mptp-induced neuronal damage mir-30e restoration abolished α-syn-triggered neuroinflammation mir-30e inhibited neuroinflammation multiple sclerosis-relevant regulator mir-30e agomir treatment major central event inhibit mptp-induced decrease including rota-rod test decreased α-syn expression rota-rod test showed turn attenuates neuroinflammation α-syn-induced neuroinflammaiton mir-30e binding site α-syn protein expression mptp-induced pd mice microrna feedback circuit negative control-treated mice glioma cells differentiation mir-30e upregulation mir-124 regulates apoptosis alpha-synuclein expression aggregated alpha-synuclein mir-30e agomir

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         headline:MicroRNA-30e regulates neuroinflammation in MPTP model of Parkinson’s disease by targeting Nlrp3
         description:Accumulating evidences suggest that neuroinflammation is a pathological hallmark of Parkinson’s disease (PD), a neurodegenerative disorder characterized by loss of dopaminergic neurons in substantia nigra pars compacta (SNpc). MicroRNAs have been recently recognized as crucial regulators of inflammatory responses. Here, we found significant downregulation of microRNA-30e (miR-30e) in SNpc of MPTP-induced PD mice. Next, we employed miR-30e agomir to upregulate miR-30e expression in MPTP-treated mice. Our results showed that delivery of miR-30e agomir remarkably improved motor behavioral deficits and neuronal activity, and inhibited the loss of dopamine neurons. Moreover, the increased α-synuclein protein expression in SNpc of MPTP-PD mice was alleviated by the upregulation of miR-30e. Further, miR-30e agomir administration also attenuated the marked increase of inflammatory cytokines, such as TNF-α, COX-2, iNOS, and restored the decreased secretion of BDNF in SNpc. In addition, we demonstrated for the first time that miR-30e directly targeted to Nlrp3, thus suppressing Nlrp3 mRNA and protein expression. Finally, miR-30e upregulation significantly inhibited the activation of Nlrp3 inflammasome as evident from the decreased Nlrp3, Caspase-1 and ASC expressions and IL-18 and IL-1β secretions. Taken together, our study demonstrates that miR-30e ameliorates neuroinflammation in the MPTP model of PD by decreasing Nlrp3 inflammasome activity. These findings suggesting that miR30e may be a key inflammation-mediated molecule that could be a potential target for PD therapeutics.
         datePublished:2017-12-22T00:00:00Z
         dateModified:2017-12-22T00:00:00Z
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ScholarlyArticle:
      headline:MicroRNA-30e regulates neuroinflammation in MPTP model of Parkinson’s disease by targeting Nlrp3
      description:Accumulating evidences suggest that neuroinflammation is a pathological hallmark of Parkinson’s disease (PD), a neurodegenerative disorder characterized by loss of dopaminergic neurons in substantia nigra pars compacta (SNpc). MicroRNAs have been recently recognized as crucial regulators of inflammatory responses. Here, we found significant downregulation of microRNA-30e (miR-30e) in SNpc of MPTP-induced PD mice. Next, we employed miR-30e agomir to upregulate miR-30e expression in MPTP-treated mice. Our results showed that delivery of miR-30e agomir remarkably improved motor behavioral deficits and neuronal activity, and inhibited the loss of dopamine neurons. Moreover, the increased α-synuclein protein expression in SNpc of MPTP-PD mice was alleviated by the upregulation of miR-30e. Further, miR-30e agomir administration also attenuated the marked increase of inflammatory cytokines, such as TNF-α, COX-2, iNOS, and restored the decreased secretion of BDNF in SNpc. In addition, we demonstrated for the first time that miR-30e directly targeted to Nlrp3, thus suppressing Nlrp3 mRNA and protein expression. Finally, miR-30e upregulation significantly inhibited the activation of Nlrp3 inflammasome as evident from the decreased Nlrp3, Caspase-1 and ASC expressions and IL-18 and IL-1β secretions. Taken together, our study demonstrates that miR-30e ameliorates neuroinflammation in the MPTP model of PD by decreasing Nlrp3 inflammasome activity. These findings suggesting that miR30e may be a key inflammation-mediated molecule that could be a potential target for PD therapeutics.
      datePublished:2017-12-22T00:00:00Z
      dateModified:2017-12-22T00:00:00Z
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         Neuroinflammation
         Neurodegeneration
         Nlrp3 inflammasome
         miR-30e
         Cell Biology
         Oncology
         Surgery
         Gynecology
         Reproductive Medicine
         Stem Cells
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