1. [Microfilaments and intermediate filaments in the fetal capillary endothelial cells of the human chorionic villi--ultrastructural and immunohistochemical study].
- Author
-
Watanabe Y
- Subjects
- Actin Cytoskeleton metabolism, Actins metabolism, Capillaries embryology, Capillaries ultrastructure, Endothelium, Vascular embryology, Endothelium, Vascular metabolism, Endothelium, Vascular ultrastructure, Female, Humans, Immunohistochemistry, Intermediate Filaments metabolism, Pre-Eclampsia metabolism, Pre-Eclampsia pathology, Pregnancy metabolism, Vimentin metabolism, Actin Cytoskeleton ultrastructure, Chorionic Villi blood supply, Cytoskeleton ultrastructure, Intermediate Filaments ultrastructure
- Abstract
Augmentation of cytoskeletons in fetal capillary endothelial cells is one of the well known pathologic changes in toxemic placentae. But we can find very few reports on these filaments in placentae, especially on their ontogeny. An ultrastructural study on human chorionic villi from 55 normal and 25 toxemic pregnancies, covering all periods of gestation, revealed that endothelial cells already had a small amount of intermediate filaments and microfilaments from 6 weeks' gestation and that they gradually increased as pregnancy progresses. In toxemic cases, intermediate filaments were markedly augmented, occasionally forming bundles, to occupy the cytoplasm of endothelial cells, so that there was often no space for cytoplasmic organelles. Intermediate filaments were predominant in thinner parts of endothelial cells; both intermediate filaments and microfilaments were easily recognized in thicker parts. These filaments seemed to determine the arrangement of organelles such as rough endoplasmic reticulum and mitochondria. Immunohistochemical and immunoelectron microscopic studies with monoclonal antibodies proved that endothelial cells contained vimentin and actin, not cytokeratin and desmin. In toxemic placentae, augmentation of intermediate filaments may disturb normal movements of endothelial cells, and may cause an increase in vascular resistance to placental microcirculation and intrauterine growth retardation in the fetus.
- Published
- 1989