HMGB1, TLR2, AND TLR4 EXPRESSION IN CELLULAR MODELS OF HUNTINGTON’S DISEASE

PALMIERI MATEO; LÓPEZ COUSELO FEDERICO; SABA JULIETA; RIVAS DIEGO; FRISER FREDERIKSEN MARÍA; CARNIGLIA LILA; DURAND DANIELA; LASAGA MERCEDES; CARUSO CARLA

Congreso; REUNIÓN CONJUNTA SAIC SAB AAFE AACYTAL 2023; 2023

Huntington’s Disease (HD) is a neurodegenerative genetic disorder caused by a CAG repeat expansion in the huntingtin gene that generates motor, cognitive, and psychiatric symptoms in humans. 3-nitropropionic acid (3NP) is a toxin that generates mitochondrial dysfunction like HD. In glial cells, oxidative stress can cause an inflammatory response. HMGB1 is a nuclear protein that regulates gene expression and participates in DNA repair. HMGB1 can bind to toll-like receptors (TLR) and trigger an inflammatory response. We investigated the expression of HMGB1 and its receptors in zQ175 knock-in mouse model of HD (HD mice). The expression of HMGB1 and its receptors was determined in cultures of astrocytes and microglia from WT and HD mice striatum and cortex. By immunocytochemistry, we demonstrated that the expression of HMGB1 and TLR4 increases in cortical HD microglia (p