Oxidative Stress Signaling in Blast TBI-Induced Tau Phosphorylation
Traumatic 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 str...
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MDPI AG,
2021-06-01T00:00:00Z.
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|---|---|---|---|
| 001 | doaj_dc7058aa9de94a4dba1718a968d74916 | ||
| 042 | |a dc | ||
| 100 | 1 | 0 | |a Chunyu Wang |e author |
| 700 | 1 | 0 | |a Changjuan Shao |e author |
| 700 | 1 | 0 | |a Li Zhang |e author |
| 700 | 1 | 0 | |a Sandra L. Siedlak |e author |
| 700 | 1 | 0 | |a James S. Meabon |e author |
| 700 | 1 | 0 | |a Elaine R. Peskind |e author |
| 700 | 1 | 0 | |a Yubing Lu |e author |
| 700 | 1 | 0 | |a Wenzhang Wang |e author |
| 700 | 1 | 0 | |a George Perry |e author |
| 700 | 1 | 0 | |a David G. Cook |e author |
| 700 | 1 | 0 | |a Xiongwei Zhu |e author |
| 245 | 0 | 0 | |a Oxidative Stress Signaling in Blast TBI-Induced Tau Phosphorylation |
| 260 | |b MDPI AG, |c 2021-06-01T00:00:00Z. | ||
| 500 | |a 10.3390/antiox10060955 | ||
| 500 | |a 2076-3921 | ||
| 520 | |a Traumatic 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 open-field 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 mitogen-activated protein kinases (MAPKs<i>)</i> 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. | ||
| 546 | |a EN | ||
| 690 | |a blast | ||
| 690 | |a traumatic brain injury | ||
| 690 | |a tau phosphorylation | ||
| 690 | |a oxidative stress | ||
| 690 | |a ERK | ||
| 690 | |a JNK | ||
| 690 | |a Therapeutics. Pharmacology | ||
| 690 | |a RM1-950 | ||
| 655 | 7 | |a article |2 local | |
| 786 | 0 | |n Antioxidants, Vol 10, Iss 6, p 955 (2021) | |
| 787 | 0 | |n https://www.mdpi.com/2076-3921/10/6/955 | |
| 787 | 0 | |n https://doaj.org/toc/2076-3921 | |
| 856 | 4 | 1 | |u https://doaj.org/article/dc7058aa9de94a4dba1718a968d74916 |z Connect to this object online. |