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Mapping Genome-wide Accessible Chromatin in Primary Human T Lymphocytes by ATAC-Seq
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ATAC-Seq analysis reveals a widespread decrease of chromatin accessibility in age-related macular degeneration.

Jie Wang1, Cristina Zibetti2, Peng Shang1,3

  • 1Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.

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|April 12, 2018
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Summary
This summary is machine-generated.

Epigenetic changes, specifically reduced chromatin accessibility in the retinal pigmented epithelium (RPE), are linked to age-related macular degeneration (AMD). HDAC11 may be a therapeutic target for this common cause of vision loss.

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Area of Science:

  • Genomics
  • Epigenetics
  • Ophthalmology

Background:

  • Age-related macular degeneration (AMD) is a leading cause of vision loss in older adults.
  • The role of epigenetic modifications in AMD pathogenesis remains largely unexplored.

Purpose of the Study:

  • To investigate global chromatin accessibility changes in the retina and RPE of AMD patients.
  • To identify epigenetic mechanisms linking environmental risk factors to AMD.

Main Methods:

  • ATAC-Seq was employed to profile chromatin accessibility in retinal and RPE samples from AMD and control individuals.
  • In vitro studies exposed RPE cells to cigarette smoke to model epigenetic changes.

Main Results:

  • Global chromatin accessibility decreased in RPE with early AMD and in the retina with advanced AMD.
  • Differentially accessible regions (DARs) were enriched for RPE/photoreceptor transcription factor binding sites, with associated gene expression alterations.
  • Cigarette smoke exposure mimicked AMD-associated chromatin changes in RPE cells.
  • HDAC11 overexpression correlated with reduced chromatin accessibility, suggesting its involvement in AMD pathology.

Conclusions:

  • Epigenetic alterations, particularly in RPE chromatin accessibility, are implicated in AMD onset and progression.
  • Cigarette smoke exposure induces epigenetic changes relevant to AMD.
  • HDAC11 represents a potential therapeutic target for mitigating AMD progression.