POSSIBLE ROLE OF TRPV-1 AND AQPS IN THE REGULATION OF TROPHOBLAST CELL VOLUME

MARTÍNEZ N,; REPPETTI J ; ABAN C; MOYA G; FARINA M; DAMIANO A

Simposio; VI LatinAmerican Symposium on Maternal-Fetal Interaction & Placenta; 2015

Mammalian cells have homeostatic mechanisms that maintain body-fluidosmolality near 300 mOsm/kg through the intake or excretion of waterand salts. This osmoregulation is vital to prevent changes in cell volumethat result in irreversible damage.Transient receptor potential vanilloid type-1 (TRPV-1) is a cation channelthat mediates Ca2+ influx in response to osmotic stress, acting as a hypertonicitysensor. Recently, we have described TRPV-1 in trophoblast cells.Aquaporins (AQPs) are a family of small integral membrane proteins thatfacilitate osmotically driven water transport. Although AQP1, AQP3 andAQP9 are highly expressed in trophoblasts during early gestation, their roleis still unknown.Objective: To evaluate the contribution of AQPs and TRPV-1 in cell volumeregulation of first trimester trophoblast and the consequences on cellviability.Methods: TRPV-1, AQP3 and AQP9 protein expressions were analyzed byWestern blot and immunohistochemistry in first trimester human chorionicvillous samples (CVS) and in the Swan-71 cell line. The effect ofhyperosmolarity on each protein expression was evaluated in Swan-71cells before and after the inhibition of AQPs with HgCl2. Cell viability wasanalyzed by MTT assay and cleaved caspase-3 expression.Results: TRPV-1, AQP3 and AQP9 expression was found in CVS and Swan-71 cells. After exposure to hyperosmolarity, we observed that theexpression of the three proteins increased (p<0.05) in Swan-71 cells. Onthe other hand, HgCl2-inhibition induced a decrease in TRPV-1 expression(p<0.05). In addition, cell viability was reduced (p<0.01) and cleavedcaspase-3 expression was increased (p<0.05) with all treatments.Conclusions: Our findings suggest that changes in the extracellular fluidosmolarity may modify TRPV-1, AQP3 and AQP9 expressions in firsttrimester trophoblast cells, inducing cell death. Therefore, we propose thatthese proteins may be involved in the regulation of trophoblast volumehomeostasis.