p47Phox/CDK5/DRP1-Mediated Mitochondrial Fission Evokes PV Cell Degeneration in the Rat Dentate Gyrus Following Status Epilepticus
Parvalbumin (PV) is one of the calcium-binding proteins, which plays an important role in the responsiveness of inhibitory neurons to an adaptation to repetitive spikes. Furthermore, PV neurons are highly vulnerable to status epilepticus (SE, prolonged seizure activity), although the underlining mec...
Ausführliche Beschreibung
Autor*in: |
Ji-Eun Kim [verfasserIn] Tae-Cheon Kang [verfasserIn] |
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Sprache: |
Englisch |
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2017 |
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Übergeordnetes Werk: |
In: Frontiers in Cellular Neuroscience - Frontiers Media S.A., 2008, 11(2017) |
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Übergeordnetes Werk: |
volume:11 ; year:2017 |
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DOI / URN: |
10.3389/fncel.2017.00267 |
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DOAJ03654289X |
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10.3389/fncel.2017.00267 doi (DE-627)DOAJ03654289X (DE-599)DOAJ931f59d24ed14ff1a168af573cac2182 DE-627 ger DE-627 rakwb eng RC321-571 Ji-Eun Kim verfasserin aut p47Phox/CDK5/DRP1-Mediated Mitochondrial Fission Evokes PV Cell Degeneration in the Rat Dentate Gyrus Following Status Epilepticus 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Parvalbumin (PV) is one of the calcium-binding proteins, which plays an important role in the responsiveness of inhibitory neurons to an adaptation to repetitive spikes. Furthermore, PV neurons are highly vulnerable to status epilepticus (SE, prolonged seizure activity), although the underlining mechanism remains to be clarified. In the present study, we found that p47Phox expression was transiently and selectively increased in PV neurons 6 h after SE. This up-regulated p47Phox expression was accompanied by excessive mitochondrial fission. In this time point, CDK5-tyrosine 15 and dynamin-related protein 1 (DRP1)-serine 616 phosphorylations were also increased in PV cells. Apocynin (a p47Phox inhibitor) effectively mitigated PV cell loss via inhibition of CDK5/DRP1 phosphorylations and mitochondrial fragmentation induced by SE. Roscovitine (a CDK5 inhibitor) and Mdivi-1 (a DRP1 inhibitor) attenuated SE-induced PV cell loss by inhibiting aberrant mitochondrial fission. These findings suggest that p47Phox/CDK5/DRP1 may be one of the important upstream signaling pathways in PV cell degeneration induced by SE via excessive mitochondrial fragmentation. apocynin epilepsy mitochondria mitochondrial fragmentation roscovitine TUNEL Neurosciences. Biological psychiatry. Neuropsychiatry Tae-Cheon Kang verfasserin aut In Frontiers in Cellular Neuroscience Frontiers Media S.A., 2008 11(2017) (DE-627)579826414 (DE-600)2452963-1 16625102 nnns volume:11 year:2017 https://doi.org/10.3389/fncel.2017.00267 kostenfrei https://doaj.org/article/931f59d24ed14ff1a168af573cac2182 kostenfrei http://journal.frontiersin.org/article/10.3389/fncel.2017.00267/full kostenfrei https://doaj.org/toc/1662-5102 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2017 |
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10.3389/fncel.2017.00267 doi (DE-627)DOAJ03654289X (DE-599)DOAJ931f59d24ed14ff1a168af573cac2182 DE-627 ger DE-627 rakwb eng RC321-571 Ji-Eun Kim verfasserin aut p47Phox/CDK5/DRP1-Mediated Mitochondrial Fission Evokes PV Cell Degeneration in the Rat Dentate Gyrus Following Status Epilepticus 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Parvalbumin (PV) is one of the calcium-binding proteins, which plays an important role in the responsiveness of inhibitory neurons to an adaptation to repetitive spikes. Furthermore, PV neurons are highly vulnerable to status epilepticus (SE, prolonged seizure activity), although the underlining mechanism remains to be clarified. In the present study, we found that p47Phox expression was transiently and selectively increased in PV neurons 6 h after SE. This up-regulated p47Phox expression was accompanied by excessive mitochondrial fission. In this time point, CDK5-tyrosine 15 and dynamin-related protein 1 (DRP1)-serine 616 phosphorylations were also increased in PV cells. Apocynin (a p47Phox inhibitor) effectively mitigated PV cell loss via inhibition of CDK5/DRP1 phosphorylations and mitochondrial fragmentation induced by SE. Roscovitine (a CDK5 inhibitor) and Mdivi-1 (a DRP1 inhibitor) attenuated SE-induced PV cell loss by inhibiting aberrant mitochondrial fission. These findings suggest that p47Phox/CDK5/DRP1 may be one of the important upstream signaling pathways in PV cell degeneration induced by SE via excessive mitochondrial fragmentation. apocynin epilepsy mitochondria mitochondrial fragmentation roscovitine TUNEL Neurosciences. Biological psychiatry. Neuropsychiatry Tae-Cheon Kang verfasserin aut In Frontiers in Cellular Neuroscience Frontiers Media S.A., 2008 11(2017) (DE-627)579826414 (DE-600)2452963-1 16625102 nnns volume:11 year:2017 https://doi.org/10.3389/fncel.2017.00267 kostenfrei https://doaj.org/article/931f59d24ed14ff1a168af573cac2182 kostenfrei http://journal.frontiersin.org/article/10.3389/fncel.2017.00267/full kostenfrei https://doaj.org/toc/1662-5102 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2017 |
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10.3389/fncel.2017.00267 doi (DE-627)DOAJ03654289X (DE-599)DOAJ931f59d24ed14ff1a168af573cac2182 DE-627 ger DE-627 rakwb eng RC321-571 Ji-Eun Kim verfasserin aut p47Phox/CDK5/DRP1-Mediated Mitochondrial Fission Evokes PV Cell Degeneration in the Rat Dentate Gyrus Following Status Epilepticus 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Parvalbumin (PV) is one of the calcium-binding proteins, which plays an important role in the responsiveness of inhibitory neurons to an adaptation to repetitive spikes. Furthermore, PV neurons are highly vulnerable to status epilepticus (SE, prolonged seizure activity), although the underlining mechanism remains to be clarified. In the present study, we found that p47Phox expression was transiently and selectively increased in PV neurons 6 h after SE. This up-regulated p47Phox expression was accompanied by excessive mitochondrial fission. In this time point, CDK5-tyrosine 15 and dynamin-related protein 1 (DRP1)-serine 616 phosphorylations were also increased in PV cells. Apocynin (a p47Phox inhibitor) effectively mitigated PV cell loss via inhibition of CDK5/DRP1 phosphorylations and mitochondrial fragmentation induced by SE. Roscovitine (a CDK5 inhibitor) and Mdivi-1 (a DRP1 inhibitor) attenuated SE-induced PV cell loss by inhibiting aberrant mitochondrial fission. These findings suggest that p47Phox/CDK5/DRP1 may be one of the important upstream signaling pathways in PV cell degeneration induced by SE via excessive mitochondrial fragmentation. apocynin epilepsy mitochondria mitochondrial fragmentation roscovitine TUNEL Neurosciences. Biological psychiatry. Neuropsychiatry Tae-Cheon Kang verfasserin aut In Frontiers in Cellular Neuroscience Frontiers Media S.A., 2008 11(2017) (DE-627)579826414 (DE-600)2452963-1 16625102 nnns volume:11 year:2017 https://doi.org/10.3389/fncel.2017.00267 kostenfrei https://doaj.org/article/931f59d24ed14ff1a168af573cac2182 kostenfrei http://journal.frontiersin.org/article/10.3389/fncel.2017.00267/full kostenfrei https://doaj.org/toc/1662-5102 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2017 |
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p47Phox/CDK5/DRP1-Mediated Mitochondrial Fission Evokes PV Cell Degeneration in the Rat Dentate Gyrus Following Status Epilepticus |
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Parvalbumin (PV) is one of the calcium-binding proteins, which plays an important role in the responsiveness of inhibitory neurons to an adaptation to repetitive spikes. Furthermore, PV neurons are highly vulnerable to status epilepticus (SE, prolonged seizure activity), although the underlining mechanism remains to be clarified. In the present study, we found that p47Phox expression was transiently and selectively increased in PV neurons 6 h after SE. This up-regulated p47Phox expression was accompanied by excessive mitochondrial fission. In this time point, CDK5-tyrosine 15 and dynamin-related protein 1 (DRP1)-serine 616 phosphorylations were also increased in PV cells. Apocynin (a p47Phox inhibitor) effectively mitigated PV cell loss via inhibition of CDK5/DRP1 phosphorylations and mitochondrial fragmentation induced by SE. Roscovitine (a CDK5 inhibitor) and Mdivi-1 (a DRP1 inhibitor) attenuated SE-induced PV cell loss by inhibiting aberrant mitochondrial fission. These findings suggest that p47Phox/CDK5/DRP1 may be one of the important upstream signaling pathways in PV cell degeneration induced by SE via excessive mitochondrial fragmentation. |
abstractGer |
Parvalbumin (PV) is one of the calcium-binding proteins, which plays an important role in the responsiveness of inhibitory neurons to an adaptation to repetitive spikes. Furthermore, PV neurons are highly vulnerable to status epilepticus (SE, prolonged seizure activity), although the underlining mechanism remains to be clarified. In the present study, we found that p47Phox expression was transiently and selectively increased in PV neurons 6 h after SE. This up-regulated p47Phox expression was accompanied by excessive mitochondrial fission. In this time point, CDK5-tyrosine 15 and dynamin-related protein 1 (DRP1)-serine 616 phosphorylations were also increased in PV cells. Apocynin (a p47Phox inhibitor) effectively mitigated PV cell loss via inhibition of CDK5/DRP1 phosphorylations and mitochondrial fragmentation induced by SE. Roscovitine (a CDK5 inhibitor) and Mdivi-1 (a DRP1 inhibitor) attenuated SE-induced PV cell loss by inhibiting aberrant mitochondrial fission. These findings suggest that p47Phox/CDK5/DRP1 may be one of the important upstream signaling pathways in PV cell degeneration induced by SE via excessive mitochondrial fragmentation. |
abstract_unstemmed |
Parvalbumin (PV) is one of the calcium-binding proteins, which plays an important role in the responsiveness of inhibitory neurons to an adaptation to repetitive spikes. Furthermore, PV neurons are highly vulnerable to status epilepticus (SE, prolonged seizure activity), although the underlining mechanism remains to be clarified. In the present study, we found that p47Phox expression was transiently and selectively increased in PV neurons 6 h after SE. This up-regulated p47Phox expression was accompanied by excessive mitochondrial fission. In this time point, CDK5-tyrosine 15 and dynamin-related protein 1 (DRP1)-serine 616 phosphorylations were also increased in PV cells. Apocynin (a p47Phox inhibitor) effectively mitigated PV cell loss via inhibition of CDK5/DRP1 phosphorylations and mitochondrial fragmentation induced by SE. Roscovitine (a CDK5 inhibitor) and Mdivi-1 (a DRP1 inhibitor) attenuated SE-induced PV cell loss by inhibiting aberrant mitochondrial fission. These findings suggest that p47Phox/CDK5/DRP1 may be one of the important upstream signaling pathways in PV cell degeneration induced by SE via excessive mitochondrial fragmentation. |
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p47Phox/CDK5/DRP1-Mediated Mitochondrial Fission Evokes PV Cell Degeneration in the Rat Dentate Gyrus Following Status Epilepticus |
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