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Circular RNA SESN2 aggravates gestational trophoblast cell damage induced by high glucose by binding to IGF2BP2

Xin Huang1, Linlin Guo1

  • 1Department of Obstetrics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China.

Molecular Reproduction and Development
|January 9, 2023
PubMed

Insights

Circular RNA circSESN2 worsens high glucose damage in gestational diabetes mellitus by interacting with IGF2BP2. This interaction promotes trophoblast cell injury, inflammation, and oxidative stress, highlighting circSESN2 as a potential therapeutic target for GDM complications.

Area of Science:

  • Reproductive Biology
  • Molecular Biology
  • Endocrinology

Background:

  • Gestational diabetes mellitus (GDM) poses significant risks to maternal and fetal health.
  • Circular RNAs (circRNAs) are emerging as key regulators in GDM pathogenesis and potential biomarkers.
  • circRNAs influence trophoblast cell function, critical for placental development.

Purpose of the Study:

  • To investigate the role of circSESN2 in high glucose (HG)-induced trophoblast cell damage.
  • To elucidate the interaction between circSESN2 and IGF2BP2 in the context of GDM.
  • To assess the therapeutic potential of targeting circSESN2 in GDM.

Main Methods:

  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot to detect circSESN2 and IGF2BP2 levels in GDM patients.
  • In vitro experiments using HTR-8/SVneo cells treated with high glucose and transduced with circSESN2 or IGF2BP2 knockdown vectors.
  • Cell viability (MTT assay), migration (scratch test), invasion (Transwell assay), inflammatory cytokine levels (ELISA), oxidative stress markers (MDA, SOD, DCFH-DA probes), and RNA-protein binding assays (RNA pulldown, RIP) were performed.

Main Results:

  • CircSESN2 and IGF2BP2 were found to be overexpressed in GDM patients.
  • Knockdown of circSESN2 or IGF2BP2 improved cell invasion, migration, and reduced apoptosis and inflammation in HG-treated cells.
  • CircSESN2 directly binds to IGF2BP2, and IGF2BP2 overexpression exacerbates HG-induced trophoblast cell damage, even with circSESN2 knockdown.

Conclusions:

  • CircSESN2 exacerbates high glucose-induced trophoblast cell damage in GDM.
  • The mechanism involves circSESN2 binding to IGF2BP2 and upregulating its protein expression.
  • CircSESN2-IGF2BP2 axis represents a potential therapeutic target for managing GDM-related complications.
Keywords:
IGF2BP2apoptosiscircular RNA SESN2gestational diabetes mellitusproliferationtrophoblast cell

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