Hepatocyte nuclear factor (HNF)-1β and its physiological importance in endometriosis (Review)

Akasaka,Juria; Uekuri,Chiaki; Shigetomi,Hiroshi; Koike,Matsuki; Kobayashi,Hiroshi

doi:10.3892/br.2012.19

Hepatocyte nuclear factor (HNF)-1β and its physiological importance in endometriosis (Review)

Authors:
- Juria Akasaka
- Chiaki Uekuri
- Hiroshi Shigetomi
- Matsuki Koike
- Hiroshi Kobayashi
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Affiliations: Department of Obstetrics and Gynecology, Nara Medical University, Nara 634-8522, Japan
Published online on: October 11, 2012 https://doi.org/10.3892/br.2012.19
Pages: 13-17

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Abstract

Endometriosis is associated with pelvic pain and female infertility. Endometriosis induces inflammation and is vulnerable to oxidative stress damage. To update and summarize the literature concerning the mechanisms that serve to protect genomic DNA from the oxidative damage, the present study reviews the English‑language literature for biochemical studies on the transcription factor hepatocyte nuclear factor (HNF)‑1β target genes. Findings demonstrated that retrograde flow of the menstrual blood might give rise to endometriosis. Iron may have a significant impact on endometriosis gene expression. HNF‑1β regulates tissue‑specific gene expression in endometriosis, as well as the expression of several genes, including CD44v9, which binds several molecules, including hyaluronan, epidermal growth factor receptor (EGFR), leukemia‑associated Rho‑guanine nucleotide exchange factor (LARG), IQ motif containing GTPase activating protein 1 (IQGAP1), macrophage migration inhibitory factor (MIF), major histocompatibility complex, class II invariant chain (CD74), cystine transporter subunit (xCT), Fas and extracellular matrix (ECM) proteins. The CD44v9 system is involved in cell migration, growth, survival, anti‑apoptosis, immune response and anti‑oxidative stress through maintaining higher levels of antioxidants. HNF‑1β may serve to alleviate damage and promote survival of cells experiencing stress by upregulating antioxidant protein expression. This review expands current knowledge on the molecular mechanisms underlying the oxidative stress protection provided by HNF‑1β and provides evidence that elevated HNF‑1β activity might be associated with the CD44v9‑dependent signaling cascades.

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