Galectin-3 released in response to traumatic brain injury acts as an alarmin orchestrating brain immune response and promoting neurodegeneration
(2017) In Scientific Reports 7.- Abstract
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... (More)
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-1β, IL-6, TNFα 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.
(Less)
- author
- organization
- publishing date
- 2017-01-27
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Scientific Reports
- volume
- 7
- article number
- 41689
- publisher
- Nature Publishing Group
- external identifiers
-
- pmid:28128358
- wos:000393020100001
- scopus:85010987773
- ISSN
- 2045-2322
- DOI
- 10.1038/srep41689
- language
- English
- LU publication?
- yes
- id
- df1ab376-b43e-40f8-8bc1-5ae697ff4077
- date added to LUP
- 2017-02-15 07:26:26
- date last changed
- 2024-04-14 04:18:34
@article{df1ab376-b43e-40f8-8bc1-5ae697ff4077,
abstract = {{<p>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-1β, IL-6, TNFα 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.</p>}},
author = {{Yip, Ping Kei and Carrillo-Jimenez, Alejandro and King, Paul and Vilalta, Anna and Nomura, Koji and Chau, Chi Cheng and Egerton, Alexander Michael Scott and Liu, Zhuo Hao and Shetty, Ashray Jayaram and Tremoleda, Jordi L. and Davies, Meirion and Deierborg, Tomas and Priestley, John V. and Brown, Guy Charles and Michael-Titus, Adina Teodora and Venero, Jose Luis and Burguillos, Miguel Angel}},
issn = {{2045-2322}},
language = {{eng}},
month = {{01}},
publisher = {{Nature Publishing Group}},
series = {{Scientific Reports}},
title = {{Galectin-3 released in response to traumatic brain injury acts as an alarmin orchestrating brain immune response and promoting neurodegeneration}},
url = {{http://dx.doi.org/10.1038/srep41689}},
doi = {{10.1038/srep41689}},
volume = {{7}},
year = {{2017}},
}