Abstract

The difficulties in designing an effective pharmacological therapy for Systemic Lupus Erythematosus (SLE) are due in part to the complexities of its pathophysiology. However, recently researchers have begun to look at the role chromatin modification plays in SLE. Chromatin modification is important in the regulation of genomic expression.

Highlights

  • The difficulties in designing an effective pharmacological therapy for Systemic Lupus Erythematosus (SLE) are due in part to the complexities of its pathophysiology

  • Our results showed that histone deacetylase (HDAC) 1 expression is significantly (p < 0.0039) elevated in lupus patients compared to controls

  • Our analysis indicated that HDAC 2 expression levels was significantly higher (p < 0.0427) in our SLE patients compared to our controls

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Summary

Introduction

The difficulties in designing an effective pharmacological therapy for Systemic Lupus Erythematosus (SLE) are due in part to the complexities of its pathophysiology. Recently researchers have begun to look at the role chromatin modification plays in SLE. Chromatin modification is important in the regulation of genomic expression. One of the essential parts of chromatin structure are the histones. Histones are responsible for binding the nucleosome and provide the entry and exit sites to DNA. A group of enzymes that have shown to play a key role in histone modification are histone deacetylases (HDACs). HDAC enzymes work on the amino terminal tail of histones. They are able to regulate gene expression by modulating histone acetylation patterns [1]. There has been increasing evidence that targeting certain classes of HDACs can provide therapeutic benefit to patients with SLE. Preclinical studies have shown that using the HDAC inhibitor (HDACi), Trichostatin A (TSA), can reduce anti-DNA autoantibody production

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