期刊
SCIENTIFIC REPORTS
卷 7, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep41689
关键词
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资金
- Spanish Ministerio de Educacion, Cultura y Deporte
- Spanish Ministerio (MINECO/FEDER, UE), Blizard Research Theme grants, Blizard Institute, Queen Mary University of London [SAF2015-64171R]
- Barts Charity Centre for Trauma Sciences (C4TS)
- Wellcome Trust Institutional Strategic Support Fund (ISSF)
- MRC [MR/L010593/1] Funding Source: UKRI
- Medical Research Council [MR/L010593/1] Funding Source: researchfish
Traumatic brain injury (TBI) is currently a major cause of morbidity and poor quality of life in Western society, with an estimate of 2.5 million people affected per year in Europe, indicating the need for advances in TBI treatment. Within the first 24 h after TBI, several inflammatory response factors become upregulated, including the lectin galectin-3. In this study, using a controlled cortical impact (CCI) model of head injury, we show a large increase in the expression of galectin-3 in microglia and also an increase in the released form of galectin-3 in the cerebrospinal fluid (CSF) 24 h after head injury. We report that galectin-3 can bind to TLR-4, and that administration of a neutralizing antibody against galectin-3 decreases the expression of IL-1 beta, IL-6, TNF alpha and NOS2 and promotes neuroprotection in the cortical and hippocampal cell populations after head injury. Long-term analysis demonstrated a significant neuroprotection in the cortical region in the galectin-3 knockout animals in response to TBI. These results suggest that following head trauma, released galectin-3 may act as an alarmin, binding, among other proteins, to TLR-4 and promoting inflammation and neuronal loss. Taking all together, galectin-3 emerges as a clinically relevant target for TBI therapy.
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