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<p>Several microRNAs play vital roles in placental development. <i>miR-155</i> has been implicated in placental development and can directly interact with a variety of targets, including angiotensin type II receptor 1 (AT<sub>1</sub>R) (<i>Agtr1</i>) mRNA. The AT<sub>1</sub>R is pro-proliferative and promotes early placental development. We therefore tested the hypothesis that <i>miR-155</i> downregulates <i>Agtr1</i> mRNA expression and impairs placental development. Placentae and fetuses from wild-type C57Bl/6 mice (<i>miR-155</i><sup>+/+</sup>, control) and C57Bl/6 mice with a null mutation in <i>miR-155</i> (<i>miR155</i><sup>-/-</sup>) were mated with males of the same genotype and analyzed on gestational day 18.5, when placental morphology and <i>miR-155</i> and <i>AGTR1</i> expression were assessed. Additionally, HTR8/SVneo cells were cultured with a <i>miR-155</i> mimic to determine the effects on trophoblast proliferation, migration and invasion. <i>miR-155</i><sup>-/-</sup> dams produced significantly heavier pups with unchanged placental weights and fetal-to-placental weight ratios. Placentae from miR-155<sup>-/-</sup> dams had significantly larger labyrinth zones and labyrinth-to-placental area ratios than controls, with altered stereological parameters. Placental <i>Agtr1</i> mRNA and AGTR1 protein levels were significantly increased in <i>miR-155</i><sup>-/-</sup> dams. Finally, in vitro treatment in human HTR-8/SVneo cells with the <i>miR-155</i> mimic increased <i>miR-155</i> expression, decreased <i>AGTR1</i> mRNA levels and decreased the rates of trophoblast cell proliferation, migration and invasion. Thus, <i>miR-155</i> is demonstrated to attenuate placental development in mice. We propose that this is at least partly due to its effects on the AT<sub>1</sub>R.</p><p></p>

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miR-155 suppresses angiotensin II type 1 receptor synthesis during placental morphogenesis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月24日

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  • Anya L. Arthurs,
  • Eugenie R. Lumbers,
  • Lachlan Schofield,
  • Celine Lees,
  • Peck Y. Chin,
  • Alison S. Care,
  • Sarah A. Robertson,
  • John E. Schjenken,
  • Kirsty G. Pringle

摘要

Several microRNAs play vital roles in placental development. miR-155 has been implicated in placental development and can directly interact with a variety of targets, including angiotensin type II receptor 1 (AT1R) (Agtr1) mRNA. The AT1R is pro-proliferative and promotes early placental development. We therefore tested the hypothesis that miR-155 downregulates Agtr1 mRNA expression and impairs placental development. Placentae and fetuses from wild-type C57Bl/6 mice (miR-155+/+, control) and C57Bl/6 mice with a null mutation in miR-155 (miR155-/-) were mated with males of the same genotype and analyzed on gestational day 18.5, when placental morphology and miR-155 and AGTR1 expression were assessed. Additionally, HTR8/SVneo cells were cultured with a miR-155 mimic to determine the effects on trophoblast proliferation, migration and invasion. miR-155-/- dams produced significantly heavier pups with unchanged placental weights and fetal-to-placental weight ratios. Placentae from miR-155-/- dams had significantly larger labyrinth zones and labyrinth-to-placental area ratios than controls, with altered stereological parameters. Placental Agtr1 mRNA and AGTR1 protein levels were significantly increased in miR-155-/- dams. Finally, in vitro treatment in human HTR-8/SVneo cells with the miR-155 mimic increased miR-155 expression, decreased AGTR1 mRNA levels and decreased the rates of trophoblast cell proliferation, migration and invasion. Thus, miR-155 is demonstrated to attenuate placental development in mice. We propose that this is at least partly due to its effects on the AT1R.