The loss of endoglin promotes the invasion of extravillous trophoblasts

Yukio Mano, Tomomi Kotani, Kiyozumi Shibata, Hiroko Matsumura, Hiroyuki Tsuda, Seiji Sumigama, Eiko Yamamoto, Akira Iwase, Takeshi Senga, Fumitaka Kikkawa

Research output: Contribution to journalArticlepeer-review

31 Citations (Scopus)


Endoglin is a coreceptor for TGF-β, which is expressed in syncytiotrophoblasts. The soluble form of endoglin (sEng) has been observed to increase in the serum of preeclamptic patients. Several studies have shown that endoglin is involved in cancer invasion. However, the role of endoglin in extravillous trophoblasts (EVT), which have an invasive phenotype, remains unknown. The present studywasdesigned to investigate the expressionandrole of endoglin inhumanEVT.Wefoundthat endoglin was mainly expressed on cytotrophoblasts within the cell column during the first trimester and its expression decreased in the EVT by immunohistochemistry and immunocytochemistry. The expression of endoglin significantly increased after treatment with TGF-β1 and TGF-β3 in the human EVT cell line, HTR-8/SVneo, as detected by semiquantitative RT-PCR. To investigate the role of endoglin in EVT, the stable knockdown of endoglin was performed by lentiviral short hairpin RNA transfection into the HTR-8/SVneo cells. Although proliferation was not affected, the motility and invasiveness of the HTR-8/SVneo cells significantly increased by the knockdown of endoglin. Both the mRNA expression and secretion of urokinase-type plasminogen activator significantly increased in endoglin knockdown cells. The secretion of sEng was very low in HTR-8/SVneo, and the treatment of endoglin knockdown cells with 10 ng/ml sEng had no effect on their invasiveness. Therefore, the suppression of sEng was not involved in the increased invasiveness of endoglin knockdown cells. These results suggested that EVT increased their invasive function as a result of decreasing expression of transmembrane endoglin.

Original languageEnglish
Pages (from-to)4386-4394
Number of pages9
Issue number11
Publication statusPublished - 11-2011
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Endocrinology


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