Analysis of Lymphocytic DNA Damage in Early Multiple Sclerosis by Automated Gamma-H2AX and 53BP1 Foci Detection: A Case Control Study

PLoS One. 2016 Jan 28;11(1):e0147968. doi: 10.1371/journal.pone.0147968. eCollection 2016.

Abstract

Background: In response to DNA double-strand breaks, the histone protein H2AX becomes phosphorylated at its C-terminal serine 139 residue, referred to as γ-H2AX. Formation of γ-H2AX foci is associated with recruitment of p53-binding protein 1 (53BP1), a regulator of the cellular response to DNA double-strand breaks. γ-H2AX expression in peripheral blood mononuclear cells (PBMCs) was recently proposed as a diagnostic and disease activity marker for multiple sclerosis (MS).

Objective: To evaluate the significance of γ-H2AX and 53BP1 foci in PBMCs as diagnostic and disease activity markers in patients with clinically isolated syndrome (CIS) and early relapsing-remitting MS (RRMS) using automated γ-H2AX and 53BP1 foci detection.

Methods: Immunocytochemistry was performed on freshly isolated PBMCs of patients with CIS/early RRMS (n = 25) and healthy controls (n = 27) with γ-H2AX and 53BP1 specific antibodies. Nuclear γ-H2AX and 53BP1 foci were determined using a fully automated reading system, assessing the numbers of γ-H2AX and 53BP1 foci per total number of cells and the percentage of cells with foci. Patients underwent contrast enhanced 3 Tesla magnetic resonance imaging (MRI) and clinical examination including expanded disability status scale (EDSS) score. γ-H2AX and 53BP1 were also compared in previously frozen PBMCs of each 10 CIS/early RRMS patients with and without contrast enhancing lesions (CEL) and 10 healthy controls.

Results: The median (range) number of γ-H2AX (0.04 [0-0.5]) and 53BP1 (0.005 [0-0.2]) foci per cell in freshly isolated PBMCs across all study participants was low and similar to previously reported values of healthy individuals. For both, γ-H2AX and 53BP1, the cellular focus number as well as the percentage of positive cells did not differ between patients with CIS/RRMS and healthy controls. γ-H2AX and 53BP1 levels neither correlated with number nor volume of T2-weighted lesions on MRI, nor with the EDSS. Although γ-H2AX, but not 53BP1, levels were higher in previously frozen PBMCs of patients with than without CEL, γ-H2AX values of both groups overlapped and γ-H2AX did not correlate with the number or volume of CEL.

Conclusion: γ-H2AX and 53BP1 foci do not seem to be promising diagnostic or disease activity biomarkers in patients with early MS. Lymphocytic DNA double-strand breaks are unlikely to play a major role in the pathophysiology of MS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Biomarkers / metabolism
  • Case-Control Studies
  • DNA Damage*
  • Female
  • Histones / metabolism*
  • Humans
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Lymphocytes / metabolism*
  • Male
  • Middle Aged
  • Multiple Sclerosis / genetics*
  • Multiple Sclerosis / metabolism
  • Multiple Sclerosis / pathology
  • Tumor Suppressor p53-Binding Protein 1
  • Young Adult

Substances

  • Biomarkers
  • H2AX protein, human
  • Histones
  • Intracellular Signaling Peptides and Proteins
  • TP53BP1 protein, human
  • Tumor Suppressor p53-Binding Protein 1

Grants and funding

Support was provided by the German Ministry of Education and Research (BMBF/KKNMS, Competence Network Multiple Sclerosis, grant number 01GI1312) Charité Research Fund. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Medipan GmbH provided support in the form of salaries for authors (LH, CE, PB, and DR) and research materials. LH, CE, PB, and DR were involved in the study design, data collection and analysis, decision to publish, and preparation of the manuscript.