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HDAC1 and HDAC2 are Differentially Expressed in Endometriosis

Authors
  • Colón-Díaz, Maricarmen1
  • Báez-Vega, Perla1
  • García, Miosotis2
  • Ruiz, Abigail1
  • Monteiro, Janice B.1
  • Fourquet, Jessica1
  • Bayona, Manuel3
  • Alvarez-Garriga, Carolina3
  • Achille, Alexandra4
  • Seto, Edward4
  • Flores, Idhaliz1
  • 1 Ponce School of Medicine and Health Sciences, Ponce, PR, 00731, USA , Ponce (United States)
  • 2 Hato Rey Pathology, Inc., San Juan, PR, USA , San Juan (United States)
  • 3 Ponce School of Medicine and Health Sciences, Ponce, PR, USA , Ponce (United States)
  • 4 Molecular Oncology, H. Lee Moffitt Cancer Center, Tampa, FL, USA , Tampa (United States)
Type
Published Article
Journal
Reproductive Sciences
Publisher
SAGE Publications
Publication Date
May 01, 2012
Volume
19
Issue
5
Pages
483–492
Identifiers
DOI: 10.1177/1933719111432870
Source
Springer Nature
Keywords
License
Yellow

Abstract

Epigenetic mechanisms have been ascribed important roles in endometriosis. Covalent histone modifications at lysine residues have been shown to regulate gene expression and thus contribute to pathological states in many diseases. In endometriosis, histone deacetylase inhibition (HDACi) resulted in reactivation of E-cadherin, attenuation of invasion, decreased proliferation of endometriotic cells, and caused lesion regression in an animal model. This study was conducted to assess basal and hormone-regulated gene expression levels of HDAC1 and HDAC2 (HDAC1/2) in cell lines and protein expression levels in tissues. Basal and steroid hormone-regulated HDAC1/2 gene expression levels were determined by quantitative polymerase chain reaction in cell lines and tissues. Protein levels were measured by immunohistochemistry (IHC) in tissues on an endometriosis tissue micro-array (TMA). Basal HDAC1/2 gene expression levels were significantly higher in endometriotic versus endometrial stromal cells, which was confirmed by Western blot analysis. Estradiol (E2) and progesterone (P4) significantly downregulated HDAC1 expression in endometrial epithelial cells. Levels of HDAC2 were upregulated by E2 and downregulated by E2 + P4 in endometrial stro-mal cells. Hormone modulation of HDAC1/2 gene expression was lost in the endometriotic cell line. Immunohistochemistry showed that HDAC1/2 proteins were expressed in a substantial proportion of lesions and endometrium from patients, and their expression levels varied according to lesion localization. The highest proportion of strong HDAC1 immunostaining was seen in ovarian, skin, and gastrointestinal lesions, and of HDAC2 in skin lesions and endometrium from patients with endometriosis. These studies suggest that endometriosis etiology may be partially explained by epigenetic regulation of gene expression due to dysregulations in the expression of HDACs.

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