Protease-activated receptor 2 contributes to placental development and fetal growth in mice

Shu Yamakage, Yuji Oe, Akiyo Sekimoto, Hirofumi Obata, Miho Yasuta, Emiko Sato, Satoshi Kumakura, Hiroshi Sato, Junichi Sugawara, Sadayoshi Ito, Nobuyuki Takahashi

研究成果: Article査読

1 被引用数 (Scopus)

抄録

Background: Protease-activated receptor 2 (PAR2) is activated by serine proteases such as coagulation tissue factor/VIIa complex, factor Xa or trypsin and is pro-angiogenic in several disease models. Impaired angiogenesis in placenta causes placental dysfunction and fetal growth restriction. PAR2 is expressed in the placenta trophoblast. However, the role of PAR2 in pregnancy remains unknown. Objective: The present study aimed to examine the role of PAR2 in placental development and fetal growth using a murine model. Methods: PAR2−/− or PAR2+/+ mice in the ICR background were used. Female PAR2−/− mice were mated with male PAR2−/− mice, and female PAR2+/+ mice were mated with male PAR2+/+ mice to obtain PAR2−/− and PAR2+/+ fetuses, respectively. The day a virginal plug was observed in the morning was determined as 0.5-day post-coitum (dpc). Pregnant mice were sacrificed on 13.5 or 18.5 dpc to collect samples. Results: A deficiency of PAR2 significantly reduced the fetal and placental weight and impaired placental labyrinth development in mice on 18.5 dpc. Collagen IV expression in placenta labyrinth was smaller in PAR2 knockout mice compared to that of wild-type mice. A deficiency of PAR2 also reduced the expression levels of genes related to angiogenesis and coagulation in placenta. Conclusion: Our data suggest that PAR2 is required for fetal growth and angiogenesis in the placenta and is thus important for a normal pregnancy.

本文言語English
ページ(範囲)173-179
ページ数7
ジャーナルThrombosis Research
193
DOI
出版ステータスPublished - 2020 9

ASJC Scopus subject areas

  • 血液学

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