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Differential expression and inhibitory effects of aquaporins on the development of adenomyosis

Liping Jia1, Yuzhu Liu1, Yixu Han1

  • 1Department of Gynecology, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570311, P.R. China.

Molecular Medicine Reports
|September 9, 2020
PubMed

Insights

Aquaporin 5 (AQP5) silencing may suppress adenomyosis (AM) by reducing cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT). AQP2, AQP5, and AQP8 are highly expressed in AM tissues.

Area of Science:

  • Reproductive Biology
  • Molecular Biology
  • Cell Biology

Background:

  • Adenomyosis (AM) is a gynecological condition characterized by the presence of endometrial tissue within the myometrium.
  • Aquaporins (AQPs), specifically AQP2, AQP5, and AQP8, are implicated in AM pathogenesis, but their precise roles require further elucidation.

Purpose of the Study:

  • To investigate the roles of AQP2, AQP5, and AQP8 in a mouse model of adenomyosis.
  • To determine the effect of AQP5 silencing on the viability, migration, and invasion of endometrial stromal cells (ESCs) from patients with AM.

Main Methods:

  • Establishment of an AM mouse model using Institute of Cancer Research (ICR) female mice.
  • Histopathological analysis (hematoxylin-eosin staining) and quantification of AM severity.
  • Isolation and characterization of human eutopic and ectopic ESCs.
  • Assessment of ESCs' viability, migration, and invasion following AQP5 silencing (siAQP5) using Cell Counting Kit-8, scratch wound-healing, and Transwell assays.
  • Analysis of mRNA and protein expression levels of AQP5, EMT markers (E-cadherin, N-cadherin), MMP-2, and MMP-9 via RT-qPCR and Western blotting.

Main Results:

  • The AM mouse model exhibited increased AM severity, uterus index, and uterine surface nodules compared to the sham group.
  • AQP2, AQP5, and AQP8 proteins were upregulated in both eutopic and ectopic endometrium of AM mice, with AQP5 showing higher expression.
  • AQP5 silencing in human ESCs significantly reduced cell viability, migration, invasion, and suppressed the expression of EMT markers and MMP-2/MMP-9.

Conclusions:

  • AQP2, AQP5, and AQP8 are highly expressed in the eutopic and ectopic endometrium of adenomyosis.
  • AQP5 plays a critical role in promoting cell viability, migration, invasion, and epithelial-mesenchymal transition in ESCs.
  • Targeting AQP5 may represent a potential therapeutic strategy for suppressing adenomyosis progression.

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