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Abnormal expression of Nrf2 may play an important role in the pathogenesis and development of adenomyosis

Ning Chen1, Baoying Du1, Hao Zhou2

  • 1Department of Gynecology, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, P.R. China.

Plos One
|August 18, 2017
PubMed
Abstract

Insights

Nuclear factor erythroid 2-related factor 2 (Nrf2) protein is upregulated in adenomyosis, promoting endometrial cell migration and MMP9 expression. Targeting Nrf2 offers a potential therapeutic strategy for adenomyosis.

Area of Science:

  • Gynecology
  • Cell Biology
  • Molecular Medicine

Background:

  • Adenomyosis is a benign gynecological condition characterized by endometrial gland and stroma infiltration into the myometrium.
  • The underlying molecular mechanisms of adenomyosis pathogenesis remain incompletely understood.
  • Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator of cellular defense against oxidative stress.

Purpose of the Study:

  • To investigate the expression levels of Nrf2 in adenomyosis tissues.
  • To elucidate the role of Nrf2 in the pathogenesis and cellular behavior of adenomyosis.
  • To explore the potential of Nrf2 as a therapeutic target for adenomyosis.

Main Methods:

  • Western blot and immunohistochemistry (IHC) were employed to quantify Nrf2 protein levels in tissue samples.
  • Real-time PCR was utilized to assess Nrf2 mRNA expression.
  • In vitro experiments involved Nrf2 knockdown and overexpression in primary endometrial glandular cells to evaluate migration and MMP9 expression.

Main Results:

  • Nrf2 protein levels were significantly elevated in both eutopic and ectopic endometrial glands of adenomyosis patients compared to controls.
  • No significant difference in Nrf2 mRNA levels was observed between adenomyosis and control groups.
  • Modulating Nrf2 protein levels in cultured cells affected cell migration and matrix metalloproteinase 9 (MMP9) expression, with higher Nrf2 correlating with increased migration and MMP9 levels.

Conclusions:

  • Abnormal Nrf2 protein expression is implicated in the pathogenesis and progression of adenomyosis.
  • Nrf2 influences the migratory capacity of endometrial glandular cells, potentially via MMP9 regulation.
  • Targeting Nrf2, specifically by reducing its expression, presents a promising therapeutic avenue for adenomyosis treatment.

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