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Egr-ly awaiting a "personalized medicine" approach to treat scleroderma

Andrew Leask1

  • 1Departments of Dentistry and Physiology and Pharmacology, Dental Sciences Building, University of Western Ontario, London, ON, Canada, N6A 5C1, Andrew.leask@schulich.uwo.ca.

Journal of Cell Communication and Signaling
|February 22, 2012
PubMed

Insights

Scleroderma, a fibrotic autoimmune disease, shows heterogeneity. Targeting transcription factor Early growth response (Egr)-1 may treat diffuse scleroderma fibrosis, while targeting interleukin-13 (IL-13) may address localized scleroderma inflammation.

Area of Science:

  • Immunology
  • Dermatology
  • Genetics

Background:

  • Scleroderma is an autoimmune disorder causing skin and organ fibrosis with no effective treatments.
  • Despite research, clinical trial outcomes for scleroderma have been poor, likely due to disease heterogeneity.
  • Genome-wide expression profiling reveals molecular insights into scleroderma's diverse mechanisms.

Purpose of the Study:

  • To investigate the molecular drivers of fibrosis and inflammation in different scleroderma subtypes.
  • To explore the roles of transcription factor Early growth response (Egr)-1 and interleukin-13 (IL-13) in scleroderma pathogenesis.
  • To identify potential therapeutic targets for distinct scleroderma patient groups.

Main Methods:

  • Analysis of gene expression profiles in scleroderma patients.
  • Comparison of gene expression patterns between diffuse cutaneous scleroderma, localized scleroderma, and murine sclerodermatous graft-versus-host disease (sclGVHD).
  • Evaluation of the regulatory roles of Egr-1 and TGF-ß, and IL-13 in scleroderma-associated gene expression.

Main Results:

  • Overexpression of "fibroproliferative" genes in diffuse cutaneous scleroderma is linked to Early growth response (Egr)-1.
  • Only a subset of Egr-1-regulated genes are also regulated by TGF-ß.
  • Overexpression of "inflammatory" genes in localized scleroderma is associated with interleukin-13 (IL-13) activity.
  • Murine sclGVHD gene expression profiles resemble the inflammatory subset of scleroderma.

Conclusions:

  • Targeting Egr-1 may offer a novel therapeutic strategy for fibrosis in a subset of diffuse scleroderma patients.
  • Elevated TGF-ß signaling alone is insufficient to explain scleroderma fibrosis.
  • Targeting IL-13 could be a therapeutic approach for inflammation in localized scleroderma.

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