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Updated: Oct 17, 2025

A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta
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Circulating Exosomal miR-221 from Maternal Obesity Inhibits Angiogenesis via Targeting Angptl2.

Yuanfei Zhou1, Mao Xia1, Chenbin Cui1

  • 1Department of Animal Nutrition and Feed Science, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, China.

International Journal of Molecular Sciences
|October 13, 2021
PubMed
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Maternal obesity releases exosomes with miR-221 from adipose tissue, inhibiting placental blood vessel formation and harming fetus development. This reveals a new mechanism for obesity-related pregnancy complications.

Keywords:
angiogenesiscirculating exosomematernal obesitymiR-221

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Area of Science:

  • Obstetrics and Gynecology
  • Cell Biology
  • Endocrinology

Background:

  • Maternal obesity negatively impacts placental and fetal development.
  • The interaction between adipocytes and endothelial cells in obesity is not fully understood.
  • Exosomes mediate intercellular communication and may play a role in obesity-related complications.

Purpose of the Study:

  • To characterize exosome-enriched microRNAs (miRNAs) from obese sow adipose tissue.
  • To evaluate the effect of these exosomes on endothelial cell angiogenesis.
  • To elucidate the specific miRNA and its mechanism of action.

Main Methods:

  • Isolation and analysis of plasma exosomes using nanoparticle tracking analysis (NTA), electron microscopy, and protein marker expression.
  • miRNA profiling to identify differentially expressed miRNAs.
  • In vitro assays to assess endothelial cell migration, proliferation, and angiogenesis.
  • Validation of miRNA targets using 3' untranslated region (UTR) assays.

Main Results:

  • Exosome concentration increased with sow gestation.
  • Exosomes from obese sows inhibited endothelial cell migration and angiogenesis.
  • miR-221 was significantly enriched in exosomes from obese sows.
  • Exosomal miR-221 repressed endothelial cell proliferation and angiogenesis by targeting Angptl2's 3' UTR.

Conclusions:

  • Adipocyte-derived exosomes, particularly miR-221, mediate inhibitory effects on angiogenesis.
  • This study identifies a novel mechanism by which obesity-induced exosome secretion contributes to placental dysplasia.
  • miR-221 is a key mediator in exosome-driven angiogenesis inhibition during maternal obesity.