Table 2.
Galectins in non-MS-related CNS injuries
| Galectin | Model | Main result | Mechanism | References |
|---|---|---|---|---|
| In vivo | ||||
| gal-1 | Spinal cord injury (treatment) | Promotes axonal regeneration in Lgals1−/− C57BL/6 mice (only dimeric form) | Inhibits Sema3A binding to NRP-1–PlexinA4 complex | [215] |
| gal-1 | Epileptic seizure model (Lgals 1−/− 129 P3/J mice) | Reduced proliferation of neural progenitors | Astrocyte-secreted gal-1 may act as a growth-stimulating factor and/or increase the supply of neurotrophic factors | [219] |
|
gal-1 gal-3 |
Stab wound injury (Lgals 1−/−Lgals3−/− C57BL/6 mice) | Reduced reactive astrocyte proliferation and their NSC potential | May regulate cell cycle progression at the G1–S-phase transition | [322] |
| gal-3 | Acute ischemia (gal-3 null mutant C57Bl/6 mice) | Defective microglia activation and decreased proliferation | Required for the induction of an TLR2 response, binds to IGFR and essential for IGF1-mediated proliferation | [169] |
| gal-3 | Neonatal hypoxia–ischemia (Lgals3−/− SV129 mice) | Protected from injury particular in male mice | Increased accumulation of microglia, decreased levels of MMP-9 and less oxidative stress in the absence of gal-3 | [323] |
| gal-3 | Severe transient forebrain ischemia (male Mongolian gerbils) | Increased galectin-3 expression in microglia after the onset of neuronal damage in the hippocampal CA1 region | Not a trigger of neuronal death, hypothermia prevents gal-3 expression | [324] |
| gal-3 | Spinal cord injury (Lgals3−/− C57BL/6 mice) | Increased neurological recovery | Sustains a pro-inflammatory microglia/macrophages phenotype | [281] |
CA cornu ammonis (hippocampus), CNS central nervous system, gal galectin, Iba-1 ionized calcium-binding adaptor molecule 1, IGF insulin-like growth factor, IGFR insulin-like growth factor receptor, MMP matrix metalloproteinase, NP-1 neuropilin-1, TLR2 Toll-like receptor 2