RT Journal Article
T1 Galectin-3 released in response to traumatic brain injury acts as an alarmin orchestrating brain immune response and promoting neurodegeneration.
A1 Yip, Ping Kei
A1 Carrillo-Jimenez, Alejandro
A1 King, Paul
A1 Vilalta, Anna
A1 Nomura, Koji
A1 Chau, Chi Cheng
A1 Egerton, Alexander Michael Scott
A1 Liu, Zhuo-Hao
A1 Shetty, Ashray Jayaram
A1 Tremoleda, Jordi L
A1 Davies, Meirion
A1 Deierborg, Tomas
A1 Priestley, John V
A1 Brown, Guy Charles
A1 Michael-Titus, Adina Teodora
A1 Venero, Jose Luis
A1 Burguillos, Miguel Angel
AB 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.
YR 2017
FD 2017-01-27
LK http://hdl.handle.net/10668/10813
UL http://hdl.handle.net/10668/10813
LA en
DS RISalud
RD Apr 7, 2025