The absence of CB1 receptor reduces FAAH activity in an LPS-induced murine model of preterm delivery.

MARVALDI, CAROLINA; AISEMBERG, JULIETA; FRANCHI, ANA MARIA; WOLFSON, MANUEL LUIS

Mar del Plata

Congreso; Reunion anual de sociedades de biociencias; 2022

Preterm delivery (PTD) is the leading cause of morbi-mortality inneonates. The endocannabinoid system (eCS) is one of severalsignaling pathways involved in physiopathology of reproduction. Itcomprises the main endogenous ligand anandamide (AEA), receptors CB1, CB2 and TRPV1, biosynthesizing enzyme NAPE-PLD andthe catabolizing enzyme FAAH. Several studies have shown thatFAAH is the key player in regulating AEA levels. Previous worksfrom our lab have demonstrated that maternal LPS administrationaltered FAAH activity in deciduas and peripheral blood mononuclearcells (PBMC), resulting in embryo resorption. In our LPS-inducedmurine model of preterm delivery, we observed that the eCS of boththe decidua and PBMC is involved in triggering a PTD. We alsodemonstrated that CB1-KO mice presented a lower PTD rate whencompared to WT mice. Therefore, the aim of this study was to investigate whether the lack of CB1 receptor produces an imbalance inthe decidual eCS, we well as its effects in deciduas exposed to aninflammatory model of PTD. We studied whether LPS treatment altered the eCS in the deciduas from CB1-KO mice on day 15 of gestation. We observed that LPS treatment diminished CB2 receptorprotein levels in these mice (p