Microglia cells, the immune cells residing in the brain, express immune regulatory
molecules that have a central role in the manifestation of age-related brain characteristics.
Our hypothesis suggests that galectin-1, an anti-inflammatory member of the beta-galactoside-binding
lectin family, regulates microglia and neuroinflammation in the aging brain. Through
our in-silico analysis, we discovered a subcluster of microglia in the aged mouse
brain that exhibited increased expression of galectin-1 mRNA. In our Western blotting
experiments, we observed a decrease in galectin-1 protein content in our rat primary
cortical cultures over time. Additionally, we found that the presence of lipopolysaccharide,
an immune activator, significantly increased the expression of galectin-1 protein
in microglial cells. Utilizing flow cytometry, we determined that a portion of the
galectin-1 protein was localized on the surface of the microglial cells. As cultivation
time increased, we observed a decrease in the expression of activation-coupled molecules
in microglial cells, indicating cellular exhaustion. In our mixed rat primary cortical
cell cultures, we noted a transition of amoeboid microglial cells labeled with OX42(CD11b/c)
to a ramified, branched phenotype during extended cultivation, accompanied by a complete
disappearance of galectin-1 expression. By analyzing the transcriptome of a distinct
microglial subpopulation in an animal model of aging, we established a correlation
between chronological aging and galectin-1 expression. Furthermore, our in vitro study
demonstrated that galectin-1 expression is associated with the functional activation
state of microglial cells exhibiting specific amoeboid morphological characteristics.
Based on our findings, we identify galectin-1 as a marker for microglia activation
in the context of aging.
