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

Anya L Arthurs1,2, Eugenie R Lumbers3,4, Lachlan Schofield3,4

  • 1Flinders University, College of Medicine and Public Health, Flinders Health and Medical Research Institute, Adelaide, SA, Australia.

Cell Death Discovery
|December 24, 2025
PubMed

Insights

MicroRNA-155 (miR-155) normally limits placental development by downregulating angiotensin II type 1 receptor (AT1R). Loss of miR-155 in mice leads to larger placentas and impaired fetal growth, suggesting miR-155

Area of Science:

  • Reproductive biology and developmental science.
  • Molecular endocrinology and microRNA research.
  • Genetics and developmental biology.

Background:

  • MicroRNAs (miRNAs) are critical regulators of placental development.
  • miR-155 is known to influence placental development and targets angiotensin II type 1 receptor (AT1R) mRNA.
  • AT1R promotes proliferation and early placental growth.

Purpose of the Study:

  • To investigate the hypothesis that miR-155 downregulates Agtr1 mRNA expression and impairs placental development.
  • To elucidate the role of miR-155 in regulating placental morphology and function.
  • To determine the impact of miR-155 on trophoblast cell behavior.

Main Methods:

  • Comparative analysis of placentae and fetuses from wild-type (miR-155+/+) and miR-155 knockout (miR-155-/-) mice on gestational day 18.5.
  • Assessment of placental morphology, stereological parameters, and expression of miR-155 and AGTR1 (mRNA and protein).
  • In vitro studies using HTR8/SVneo cells treated with a miR-155 mimic to evaluate effects on trophoblast proliferation, migration, and invasion.

Main Results:

  • miR-155-/- dams exhibited significantly heavier pups, but unchanged placental weights and fetal-to-placental weight ratios.
  • Placentae from miR-155-/- dams showed larger labyrinth zones and altered stereological parameters.
  • Increased placental Agtr1 mRNA and AGTR1 protein levels were observed in miR-155-/- mice, while in vitro miR-155 mimic treatment reduced AGTR1 mRNA and trophoblast cell proliferation, migration, and invasion.

Conclusions:

  • miR-155 attenuates placental development in mice, partly through its regulation of the AT1R pathway.
  • The findings suggest a crucial role for miR-155 in balancing placental growth and function.
  • miR-155 acts as a negative regulator of trophoblast proliferation, migration, and invasion via AT1R.

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