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

PALMIERI, MATEO; LOPEZ COUSELO FEDERICO; JULIETA SABA; RIVAS, DIEGO; MARIA FRISER FREDERIKSEN; CARNIGLIA, LILA; DANIELA DURAND; LASAGA, MERCEDES; CARLA CARUSO

Mar del Plata

Congreso; Reunion conjunta SAIC SAI AAFE Nanormed.ar; 2023

SAIC

Huntington’s Disease (HD) is a neurodegenerative genetic disorder caused by a CAGrepeat expansion in the huntingtin gene that generates motor, cognitive, and psychiatricsymptoms in humans. 3-nitropropionic acid (3NP) is a toxin that generatesmitochondrial dysfunction like HD. In glial cells, oxidative stress can cause aninflammatory response. HMGB1 is a nuclear protein that regulates gene expression andparticipates in DNA repair. HMGB1 can bind to toll-like receptors (TLR) and trigger aninflammatory response. We investigated the expression of HMGB1 and its receptors inzQ175 knock-in mouse model of HD (HD mice). The expression of HMGB1 and itsreceptors was determined in cultures of astrocytes and microglia from WT and HD micestriatum and cortex. By immunocytochemistry, we demonstrated that the expression ofHMGB1 and TLR4 increases in cortical HD microglia (p