Localization of micro- and intermediate filaments in non-pregnant uterus and placenta of the mink suggests involvement of maternal endothelial cells and periendothelial cells in blood flow regulation

Abstract

 Maternal stem arteries and arterioles of the endotheliochorial mink placenta have been shown to lack smooth muscle cells, suggesting a muscle-free attenuation of the maternal arterial pulse wave of the placenta. Since the endotheliochorial type of placenta by definition does not contain any maternal supportive tissue (e.g. connective tissue), except for the specialized interstitial layer, the aim of this study was to reveal cytoskeletal components able to compensate for the lack of conventional regulatory mechanisms of maternal placental blood flow. The study was undertaken on buffered formalin fixed tissues from 19 minks by immunohistochemistry and transmission electron microscopy to localize three major cytoskeletal filaments (desmin, vimentin and α-smooth muscle actin (α-sm-actin)) in non-pregnant uteri and placenta. The contractile α-sm-actin was immunodetected in the maternal subepithelial and periglandular connective tissue cells of the cyclic endometrium and during early gestation. During the transition from early- to mid gestation, maternal periendothelial cells appeared and showed α-sm-actin immuno-positivity; however, in late gestation, this activity could not be detected because the periendothelial cells had disappeared. Fetal endothelial cells displayed intense α-sm-actin immunoreactivity, which was in contrast to the α-sm-actin negative maternal endothelial cells. Allantochorionic mesenchymal cells also exhibited intense α-sm-actin immunostaining. Vimentin was immunohistochemically expressed in endothelial cells (maternal as well as fetal), maternal periendothelial cells, allantochorionic mesenchymal cells, and maternal connective tissue cells from early gestation. Desmin was not immunohistochemically detectable in cyclic endometrium and placental tissues. Transmission electron microscopy revealed the periendothelial cells to be enclosed by a thin interstitial layer. Additionally, the maternal endothelial cells displayed actin myofilament-like structures anchored basally. From our data we conclude that maternal periendothelial cells, immunoreactive for contractile actin, and maternal endothelial cells, possessing actin myofilament-like ultrastructures, act as supportive systems in the maternal vessel walls, probably influencing the regulation of the maternal blood flow.