Oxidative Stress Signaling in Blast TBI-Induced Tau Phosphorylation

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dc.contributor.authorWang, Chunyu
dc.contributor.authorShao, Changjuan
dc.contributor.authorZhang, Li
dc.contributor.authorSiedlak, Sandra L.
dc.contributor.authorMeabon, James S.
dc.contributor.authorPeskind, Elaine R.
dc.contributor.authorLu, Yubing
dc.contributor.authorWang, Wenzhang
dc.contributor.authorPerry, George
dc.contributor.authorCook, David G.
dc.contributor.authorZhu, Xiongwei
dc.date.accessioned2021-06-24T14:10:44Z
dc.date.available2021-06-24T14:10:44Z
dc.date.issued2021-06-15
dc.date.updated2021-06-24T14:10:45Z
dc.description.abstractTraumatic brain injury caused by blast is associated with long-term neuropathological changes including tau phosphorylation and pathology. In this study, we aimed to determine changes in initial tau phosphorylation after exposure to a single mild blast and the potential contribution of oxidative stress response pathways. C57BL/6 mice were exposed to a single blast overpressure (BOP) generated by a compressed gas-driven shock tube that recapitulates battlefield-relevant openfield BOP, and cortical tissues were harvested at different time points up to 24 h after blast for Western blot analysis. We found that BOP caused elevated tau phosphorylation at Ser202/Thr205 detected by the AT8 antibody at 1 h post-blast followed by tau phosphorylation at additional sites (Ser262 and Ser396/Ser404 detected by PHF1 antibody) and conformational changes detected by Alz50 antibody. BOP also induced acute oxidative damage at 1 h post-blast and gradually declined overtime. Interestingly, Extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) were acutely activated in a similar temporal pattern as the rise and fall in oxidative stress after blast, with p38 showing a similar trend. However, glycogen synthase kinase-3 β (GSK3β) was inhibited at 1 h and remained inhibited for 24 h post blast. These results suggested that mitogenactivated protein kinases (MAPKs) but not GSK3β are likely involved in mediating the effects of oxidative stress on the initial increase of tau phosphorylation following a single mild blast.
dc.description.departmentNeuroscience, Developmental and Regenerative Biology
dc.description.departmentChemistry
dc.identifierdoi: 10.3390/antiox10060955
dc.identifier.citationAntioxidants 10 (6): 955 (2021)
dc.identifier.urihttps://hdl.handle.net/20.500.12588/623
dc.rightsAttribution 4.0 United States
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectblast
dc.subjecttraumatic brain injury
dc.subjecttau phosphorylation
dc.subjectoxidative stress
dc.subjectERK
dc.subjectJNK
dc.subjectp38
dc.subjectGSK3?
dc.titleOxidative Stress Signaling in Blast TBI-Induced Tau Phosphorylation
dc.typeArticle

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