info:eu-repo/semantics/article
Hyperosmolarity Impairs Human Extravillous Trophoblast Differentiation by Caveolae Internalization
Fecha
2021-12Registro en:
Reppetti, Julieta; Medina Mora, Yollyseth Astrid; Farina, Mariana; Damiano, Alicia Ermelinda; Martinez, Nora Alicia; Hyperosmolarity Impairs Human Extravillous Trophoblast Differentiation by Caveolae Internalization; Frontiers Media; Frontiers in Physiology; 12; 12-2021; 1-12
1664-042X
CONICET Digital
CONICET
Autor
Reppetti, Julieta
Medina Mora, Yollyseth Astrid
Farina, Mariana
Damiano, Alicia Ermelinda
Martinez, Nora Alicia
Resumen
We recently reported that an intact caveolar structure is necessary for adequate cell migration and tubulogenesis of the human extravillous trophoblast (EVT) cells. Emerging evidence supports that hyperosmolarity induces the internalization of caveolae into the cytoplasm and accelerates their turnover. Furthermore, signaling pathways associated with the regulation of trophoblast differentiation are localized in caveolae. We hypothesized that hyperosmolarity impairs EVT differentiation and caveolae/caveolin−1 (Cav-1) participates in this process. EVT cells (Swan 71 cell line) were cultured in complete Dulbecco’s Modified Eagle Medium/Nutrient Mixture F-12 and exposed to hyperosmolar condition (generated by the addition of 100 mM sucrose). Hyperosmolarity altered the EVT cell migration and the formation of tube-like structures. In addition, cell invasion was decreased along with a reduction in the latent and active forms of matrix metalloproteinase-2 (MMP−2) secreted by these cells. With respect to Cav-1 protein abundance, we found that hyperosmolarity enhanced its degradation by the lysosomal pathway. Accordingly, in the hyperosmolar condition, we also observed a significant increase in the number of vacuoles and the internalization of the caveolae into the cytoplasm. Taken together, our findings suggest that hyperosmolarity may induce caveolae internalization and increase their turnover, compromising the normal differentiation of EVT cells.