Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5894110 | Placenta | 2016 | 30 Pages |
Abstract
During human placentation, the extravillous trophoblast (EVT) invades the maternal decidua and reconstructs maternal spiral arteries. However, the precise mechanisms that control EVT behavior have not yet been elucidated in detail. CD9 has been reported to be a cell-motility-related molecule. Since we previously observed that CD9 was expressed on human EVT, we examined the possible involvement of CD9 in the invasion process of EVT. Placental and umbilical samples were obtained from patients who underwent legal abortions, normal delivery, or hysterectomy. The expression of CD9 at the implantation site and on isolated EVT from a villous explant culture, an EVT-derived immortalized cell line, Swan71, and HUVEC was examined by immunocytochemical staining, flow cytometry, and RT-PCR. The effects of anti-CD9 functional antibody (ALB6) on EVT and Swan71Â cell invasion were further examined by matrigel invasion assay along with shRNAmir gene knockdown treatment. CD9 was highly expressed on EVT at the boundary region of EVT invasion and intravascular EVT. EVT and Swan71Â cell invasions were promoted by ALB6 or shRNAmir treatment. CD9 expression on Swan71Â cells was reduced under hypo-oxygenic conditions, while its expression was increased by the co-culture with HUVEC. These findings suggest that CD9 could attenuate EVT invasion under the influence of an oxygen environment and maternal endothelial cells, proposing that CD9 is a potential regulator of human placental formation.
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Authors
Hisanori Matsumoto, Yukiyasu Sato, Akihito Horie, Koh Suginami, Hirohiko Tani, Akira Hattori, Yoshihiko Araki, Kyosuke Kagami, Ikuo Konishi, Hiroshi Fujiwara,