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Exosomal lncRNA CHL1-AS1 Derived from Peritoneal Macrophages Promotes the Progression of Endometriosis via the

Ting Liu1, Mei Liu2, Caihua Zheng3

  • 1Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, People's Republic of China.

International Journal of Nanomedicine
|August 19, 2021
PubMed
Abstract

Insights

Exosomes from peritoneal macrophages carry lncRNA CHL1-AS1, promoting endometriosis progression by affecting target cells. This exosomal lncRNA may offer a new therapeutic target for endometriosis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Reproductive Medicine

Background:

  • Peritoneal macrophage-derived exosomes play a key role in endometriosis (EMs) development.
  • Exosomes facilitate intercellular communication through the transfer of biomolecules.
  • Understanding the specific exosomal components involved in EMs pathogenesis is crucial.

Purpose of the Study:

  • To investigate the role and mechanism of exosomal long non-coding RNA (lncRNA) CHL1-AS1 from peritoneal macrophages (pMφ) in endometriosis.
  • To elucidate how pMφ-derived exosomal lncRNA CHL1-AS1 influences ectopic endometrial stromal cells (eESCs).

Main Methods:

  • Isolation and identification of exosomes from pMφ.
  • Co-culture of exosomes with eESCs.
  • qRT-PCR to quantify lncRNA CHL1-AS1 expression and verify intercellular transfer.
  • Assessment of eESC proliferation, migration, invasion, and apoptosis.
  • Dual-luciferase reporter assay to confirm interactions between lncRNA CHL1-AS1, miR-610, and MDM2.
  • In vivo validation using an EMs xenograft model.

Main Results:

  • Exosomes from EMs-associated pMφ (EMs-pMφ-exo) were successfully isolated.
  • EMs-pMφ-exo promoted eESC proliferation, migration, and invasion while inhibiting apoptosis.
  • lncRNA CHL1-AS1 was upregulated in EMs-pMφ-exo and transferred to eESCs.
  • lncRNA CHL1-AS1 acts as a competing endogenous RNA for miR-610, upregulating MDM2.
  • Exosomal lncRNA CHL1-AS1 promotes EMs progression in vivo by increasing MDM2 expression.

Conclusions:

  • Exosomal lncRNA CHL1-AS1 derived from pMφ promotes endometriosis by enhancing eESC proliferation, migration, and invasion, and inhibiting apoptosis.
  • This effect is mediated through the downregulation of miR-610 and upregulation of MDM2.
  • Exosomal lncRNA CHL1-AS1 represents a potential therapeutic target for endometriosis.
Keywords:
MDM2endometriosisexosomeslncRNA CHL1-AS1miR-610peritoneal macrophages

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