Current perspectives on role of chromatin modifications and deacetylases in lung inflammation in COPD

Saravanan Rajendrasozhan, Hongwei Yao, Irfan Rahman

Research output: Contribution to journalLiterature reviewpeer-review

Abstract

Chromatin modifications and epigenetic regulation are critical for sustained and abnormal inflammatory response seen in lungs of patients with chronic obstructive pulmonary disease (COPD) because the activities of enzymes that regulate these epigenetic modifications are altered in response to cigarette smoke. Cigarette smoke induces chromatin modifications and epigenetic changes by causing post-translational modifications of histone acetyltransferases, and histone/non-histone deacetylases (HDACs), such as HDAC2 and sirtuin 1 (SIRT1), which leads to chromatin remodeling. In this review, we discussed the current knowledge on cigarette smoke/oxidants-induced post-translational modifications of deacetylases (HDAC2 and SIRT1), disruption of HDAC2/SIRT1-RelA/p65 corepressor complex associated with acetylation of RelA/p65, and chromatin modifications (histone H3 phospho-acetylation) leading to sustained pro-inflammatory gene transcription. Knowledge on molecular mechanisms of epigenetic changes in abnormal lung inflammation will help in understanding the pathophysiology of COPD which may lead to the development of novel epigenetic therapies in the near future.
Original languageEnglish
Pages (from-to)291-7
Number of pages7
JournalCOPD: Journal of Chronic Obstructive Pulmonary Disease
Volume6
Issue number4
DOIs
Publication statusPublished - Aug 2009

Keywords

  • COPD
  • Oxidants
  • Epigenetics
  • HDAC
  • SIRT1
  • Cigarette smoke

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