EZH2 Modulates the DNA Methylome and Controls T Cell Adhesion Through Junctional Adhesion Molecule A in Lupus Patients

Arthritis Rheumatol. 2018 Jan;70(1):98-108. doi: 10.1002/art.40338. Epub 2017 Dec 15.

Abstract

Objective: EZH2 is an epigenetic regulator that mediates H3K27 trimethylation (H3K27me3) and modulates DNA methylation. The aim of this study was to characterize the role of EZH2 in CD4+ T cells in the pathogenesis of systemic lupus erythematosus.

Methods: EZH2 expression levels were determined in CD4+ T cells isolated from lupus patients and healthy controls. The epigenetic effects of EZH2 overexpression in CD4+ T cells were evaluated using a genome-wide DNA methylation approach. Gene expression profiles and microRNAs (miRNAs) were assessed by quantitative polymerase chain reaction, while protein expression was examined by Western blotting. A cell adhesion assay was used to assess adhesion of CD4+ T cells to human microvascular endothelial cells.

Results: EZH2 and H3K27me3 levels were increased in CD4+ T cells from lupus patients compared to healthy controls. T cell production of EZH2 was down-regulated in the presence of miR-26a and miR-101, and levels of both miRNAs were reduced in lupus CD4+ T cells. Overexpression of EZH2 induced in CD4+ T cells resulted in significant DNA methylation changes. Genes involved in leukocyte adhesion and migration, including F11R (which encodes junctional adhesion molecule A [JAM-A]), became hypomethylated in CD4+ T cells when EZH2 was overexpressed. Overexpression of EZH2 resulted in increases in JAM-A expression and CD4+ T cell adhesion. Preincubation of EZH2-transfected CD4+ T cells with neutralizing antibodies against JAM-A significantly blunted cell adhesion. Similarly, CD4+ T cells from lupus patients overexpressed JAM-A and adhered significantly more to endothelial cells than to T cells from healthy controls. Blocking JAM-A or EZH2 significantly reduced the capacity of lupus CD4+ T cells to adhere to endothelial cells.

Conclusion: The results of this study identify a novel role of EZH2 in T cell adhesion mediated by epigenetic remodeling and up-regulation of JAM-A. Blockade of EZH2 or JAM-A might have therapeutic potential by acting to reduce T cell adhesion, migration, and extravasation in patients with lupus.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adult
  • Blotting, Western / methods
  • CD4-Positive T-Lymphocytes / metabolism*
  • Cell Adhesion / genetics
  • Cell Adhesion Molecules / metabolism*
  • Cell Culture Techniques
  • DNA / metabolism
  • DNA Methylation / genetics*
  • Enhancer of Zeste Homolog 2 Protein / metabolism*
  • Female
  • Gene Expression Profiling / methods
  • Gene Expression Regulation / genetics
  • Humans
  • Lupus Erythematosus, Systemic / immunology
  • Lupus Erythematosus, Systemic / metabolism*
  • MicroRNAs / metabolism
  • Middle Aged
  • Real-Time Polymerase Chain Reaction
  • Receptors, Cell Surface / metabolism*

Substances

  • Cell Adhesion Molecules
  • F11R protein, human
  • MicroRNAs
  • Receptors, Cell Surface
  • DNA
  • EZH2 protein, human
  • Enhancer of Zeste Homolog 2 Protein