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TDP-43 proteolysis is associated with astrocyte reactivity after traumatic brain injury in rodents.

Abstract：

:The aggregation and deposition of transactivation response DNA-binding protein 43 (TDP-43) in neurons and astrocytes is characteristic in a number of neurodegenerative diseases including Alzheimer's disease, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis. Nevertheless, the exact role of TDP-43 in astrocytes is unknown. Recently, TDP-43 was identified in neurons but not astrocytes after traumatic brain injury (TBI) in humans. In the present study, we evaluated TDP-43 expression and proteolysis in astrocytes in a rat model of TBI. We assessed TDP-43 fragment expression, astrocyte morphology, neuronal population numbers, and motor function after TBI with or without intracerebroventricular administration of a caspase-3 inhibitor. Motor dysfunction was observed after TBI in potential association astrocytic TDP-43 short fragment mislocalization and accumulation, astrogliosis, and neuronal loss. Notably, caspase-3 inhibition prevented these changes after TBI. Our findings suggest that TDP-43 proteolysis in astrocytes is related to astrogliosis and subsequent neuronal loss in TBI, and that TDP-43 may be an important therapeutic target for preventing motor dysfunction after TBI.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Huang CY,Lee YC,Li PC,Liliang PC,Lu K,Wang KW,Chang LC,Shiu LY,Chen MF,Sun YT,Wang HK

doi

10.1016/j.jneuroim.2017.10.011

subject

Has Abstract

pub_date

2017-12-15 00:00:00

pages

61-68

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(17)30394-6

journal_volume

313

pub_type

杂志文章

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