Proinflammatory and amyloidogenic S100A9 induced by traumatic brain injury in mouse model

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Standard

Proinflammatory and amyloidogenic S100A9 induced by traumatic brain injury in mouse model. / Wang, Chao; Iashchishyn, Igor A; Kara, John; Foderà, Vito; Vetri, Valeria; Sancataldo, Giuseppe; Marklund, Niklas; Morozova-Roche, Ludmilla A.

I: Neuroscience Letters, Vol. 699, 10.02.2019, s. 199-205.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Harvard

Wang, C, Iashchishyn, IA, Kara, J, Foderà, V, Vetri, V, Sancataldo, G, Marklund, N & Morozova-Roche, LA 2019, 'Proinflammatory and amyloidogenic S100A9 induced by traumatic brain injury in mouse model', Neuroscience Letters, vol. 699, s. 199-205. https://doi.org/10.1016/j.neulet.2019.02.012

APA

Wang, C., Iashchishyn, I. A., Kara, J., Foderà, V., Vetri, V., Sancataldo, G., Marklund, N., & Morozova-Roche, L. A. (2019). Proinflammatory and amyloidogenic S100A9 induced by traumatic brain injury in mouse model. Neuroscience Letters, 699, 199-205. https://doi.org/10.1016/j.neulet.2019.02.012

CBE

MLA

Vancouver

Author

Wang, Chao ; Iashchishyn, Igor A ; Kara, John ; Foderà, Vito ; Vetri, Valeria ; Sancataldo, Giuseppe ; Marklund, Niklas ; Morozova-Roche, Ludmilla A. / Proinflammatory and amyloidogenic S100A9 induced by traumatic brain injury in mouse model. I: Neuroscience Letters. 2019 ; Vol. 699. s. 199-205.

RIS

TY - JOUR

T1 - Proinflammatory and amyloidogenic S100A9 induced by traumatic brain injury in mouse model

AU - Wang, Chao

AU - Iashchishyn, Igor A

AU - Kara, John

AU - Foderà, Vito

AU - Vetri, Valeria

AU - Sancataldo, Giuseppe

AU - Marklund, Niklas

AU - Morozova-Roche, Ludmilla A

N1 - Copyright © 2019 Elsevier B.V. All rights reserved.

PY - 2019/2/10

Y1 - 2019/2/10

N2 - Traumatic brain injury (TBI) represents a significant risk factor for development of neurodegenerative diseases such as Alzheimer's and Parkinson's. The S100A9-driven amyloid-neuroinflammatory cascade occurring during primary and secondary TBI events can serve as a mechanistic link between TBI and Alzheimer's as demonstrated recently in the human brain tissues. Here by using immunohistochemistry in the controlled cortical impact TBI mouse model we have found pro-inflammatory S100A9 in the brain tissues of all mice on the first and third post-TBI days, while 70% of mice did not show any S100A9 presence on seventh post-TBI day similar to controls. This indicates that defensive mechanisms effectively cleared S100A9 in these mouse brain tissues during post-TBI recovery. By using sequential immunohistochemistry we have shown that S100A9 was produced by both neuronal and microglial cells. However, Aβ peptide deposits characteristic for Alzheimer's disease were not detected in any post-TBI animals. On the first and third post-TBI days S100A9 was found to aggregate intracellularly into amyloid oligomers, similar to what was previously observed in human TBI tissues. Complementary, by using Rayleigh scatting, intrinsic fluorescence and atomic force microscopy we demonstrated that in vitro S100A9 self-assembles into amyloid oligomers within minutes. Its amyloid aggregation is highly dependent on changes of environmental conditions such as variation of calcium levels, pH, temperature and reduction/oxidation, which might be relevant to perturbation of cellular and tissues homeostasis under TBI. Present results demonstrate that S100A9 induction mechanisms in TBI are similar in mice and humans, emphasizing that S100A9 is an important marker of brain injury and therefore can be a potential therapeutic target.

AB - Traumatic brain injury (TBI) represents a significant risk factor for development of neurodegenerative diseases such as Alzheimer's and Parkinson's. The S100A9-driven amyloid-neuroinflammatory cascade occurring during primary and secondary TBI events can serve as a mechanistic link between TBI and Alzheimer's as demonstrated recently in the human brain tissues. Here by using immunohistochemistry in the controlled cortical impact TBI mouse model we have found pro-inflammatory S100A9 in the brain tissues of all mice on the first and third post-TBI days, while 70% of mice did not show any S100A9 presence on seventh post-TBI day similar to controls. This indicates that defensive mechanisms effectively cleared S100A9 in these mouse brain tissues during post-TBI recovery. By using sequential immunohistochemistry we have shown that S100A9 was produced by both neuronal and microglial cells. However, Aβ peptide deposits characteristic for Alzheimer's disease were not detected in any post-TBI animals. On the first and third post-TBI days S100A9 was found to aggregate intracellularly into amyloid oligomers, similar to what was previously observed in human TBI tissues. Complementary, by using Rayleigh scatting, intrinsic fluorescence and atomic force microscopy we demonstrated that in vitro S100A9 self-assembles into amyloid oligomers within minutes. Its amyloid aggregation is highly dependent on changes of environmental conditions such as variation of calcium levels, pH, temperature and reduction/oxidation, which might be relevant to perturbation of cellular and tissues homeostasis under TBI. Present results demonstrate that S100A9 induction mechanisms in TBI are similar in mice and humans, emphasizing that S100A9 is an important marker of brain injury and therefore can be a potential therapeutic target.

U2 - 10.1016/j.neulet.2019.02.012

DO - 10.1016/j.neulet.2019.02.012

M3 - Article

C2 - 30753908

VL - 699

SP - 199

EP - 205

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

ER -