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ATAC-Seq analysis reveals a widespread decrease of chromatin accessibility in age-related macular degeneration

Author

Listed:
  • Jie Wang

    (Johns Hopkins University School of Medicine)

  • Cristina Zibetti

    (Johns Hopkins University School of Medicine)

  • Peng Shang

    (Johns Hopkins University School of Medicine
    University of Pittsburgh School of Medicine)

  • Srinivasa R. Sripathi

    (Johns Hopkins University School of Medicine)

  • Pingwu Zhang

    (Johns Hopkins University School of Medicine)

  • Marisol Cano

    (Johns Hopkins University School of Medicine)

  • Thanh Hoang

    (Johns Hopkins University School of Medicine)

  • Shuli Xia

    (Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine)

  • Hongkai Ji

    (Johns Hopkins Bloomberg School of Public Health)

  • Shannath L. Merbs

    (Johns Hopkins University School of Medicine)

  • Donald J. Zack

    (Johns Hopkins University School of Medicine)

  • James T. Handa

    (Johns Hopkins University School of Medicine)

  • Debasish Sinha

    (Johns Hopkins University School of Medicine
    University of Pittsburgh School of Medicine)

  • Seth Blackshaw

    (Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine)

  • Jiang Qian

    (Johns Hopkins University School of Medicine)

Abstract

Age-related macular degeneration (AMD) is a significant cause of vision loss in the elderly. The extent to which epigenetic changes regulate AMD progression is unclear. Here we globally profile chromatin accessibility using ATAC-Seq in the retina and retinal pigmented epithelium (RPE) from AMD and control patients. Global decreases in chromatin accessibility occur in the RPE with early AMD, and in the retina of advanced disease, suggesting that dysfunction in the RPE drives disease onset. Footprints of photoreceptor and RPE-specific transcription factors are enriched in differentially accessible regions (DARs). Genes associated with DARs show altered expression in AMD. Cigarette smoke treatment of RPE cells recapitulates chromatin accessibility changes seen in AMD, providing an epigenetic link between a known risk factor for AMD and AMD pathology. Finally, overexpression of HDAC11 is partially responsible for the observed reduction in chromatin accessibility, suggesting that HDAC11 may be a potential new therapeutic target for AMD.

Suggested Citation

  • Jie Wang & Cristina Zibetti & Peng Shang & Srinivasa R. Sripathi & Pingwu Zhang & Marisol Cano & Thanh Hoang & Shuli Xia & Hongkai Ji & Shannath L. Merbs & Donald J. Zack & James T. Handa & Debasish S, 2018. "ATAC-Seq analysis reveals a widespread decrease of chromatin accessibility in age-related macular degeneration," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03856-y
    DOI: 10.1038/s41467-018-03856-y
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    Cited by:

    1. Wei Jin & Shaoshuai Jiang & Xinyi Liu & Yi He & Tuo Li & Jingchun Ma & Zhihong Chen & Xiaomei Lu & Xinguang Liu & Weinian Shou & Guoxiang Jin & Junjun Ding & Zhongjun Zhou, 2024. "Disorganized chromatin hierarchy and stem cell aging in a male patient of atypical laminopathy-based progeria mandibuloacral dysplasia type A," Nature Communications, Nature, vol. 15(1), pages 1-21, December.
    2. Sudip Kumar Paul & Motohiko Oshima & Ashwini Patil & Masamitsu Sone & Hisaya Kato & Yoshiro Maezawa & Hiyori Kaneko & Masaki Fukuyo & Bahityar Rahmutulla & Yasuo Ouchi & Kyoko Tsujimura & Mahito Nakan, 2024. "Retrotransposons in Werner syndrome-derived macrophages trigger type I interferon-dependent inflammation in an atherosclerosis model," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    3. Sayan Ghosh & Ruchi Sharma & Sridhar Bammidi & Victoria Koontz & Mihir Nemani & Meysam Yazdankhah & Katarzyna M. Kedziora & Donna Beer Stolz & Callen T. Wallace & Cheng Yu-Wei & Jonathan Franks & Devi, 2024. "The AKT2/SIRT5/TFEB pathway as a potential therapeutic target in non-neovascular AMD," Nature Communications, Nature, vol. 15(1), pages 1-18, December.

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