Evidence map›Paper›PMID 34290335›Full record

ArticleScientific reports2021

Genome-wide chromatin accessibility analyses provide a map for enhancing optic nerve regeneration.

Wolfgang Pita-Thomas, Tassia Mangetti Gonçalves, Ajeet Kumar, Guoyan Zhao, Valeria Cavalli

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. AQP5 Regulates Corneal Nerve Distribution Through NETRIN-1 and SLIT3.Investigative ophthalmology & visual science · 2025
    Article
  5. Article
  6. Review
  7. CaeNeuro · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Epigenetic Regulation of Optic Nerve Development, Protection, and Repair.International journal of molecular sciences · 2022
    Review
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Wolfgang Pita-ThomasDepartment of Neuroscience, Washington University School of Medicine, St Louis, MO, 63110, USA.
Tassia Mangetti GonçalvesDepartment of Neuroscience, Washington University School of Medicine, St Louis, MO, 63110, USA.
Ajeet KumarDepartment of Neuroscience, Washington University School of Medicine, St Louis, MO, 63110, USA.
Guoyan ZhaoDepartment of Neuroscience, Washington University School of Medicine, St Louis, MO, 63110, USA. gzhao@wustl.edu.
Valeria CavalliDepartment of Neuroscience, Washington University School of Medicine, St Louis, MO, 63110, USA. cavalli@wustl.edu.
Washington University in St. Louis · USHope Center for Neurological Disorders · US

Funding

Multicellular Mechanisms Driving Axon RegenerationR35NS122260 · NINDS · WASHINGTON UNIVERSITY · PI Valeria Cavalli · 2021 to 2026
$4.8M
Dissect the mechanisms of selective regional vulnerability in Lewy Body Dementias via comparative snRNA-seq analysisR01NS123571 · NINDS · WASHINGTON UNIVERSITY · PI XU, JINBIN, ZHAO, GUOYAN · 2021 to 2025
$3.6M
POSTMORTEM VALIDATION OF BIOMARKERS FOR IMAGING PARKINSON DISEASER01NS092865 · NINDS · WASHINGTON UNIVERSITY · PI XU, JINBIN · 2016 to 2020
$1.7M
MECHANISMS OF CHROMATIN REMODELING PROMOTING AXON REGENERATIONR01NS096034 · NINDS · WASHINGTON UNIVERSITY · PI CAVALLI, VALERIA · 2016 to 2020
$1.7M
IDENTIFYING EPIGENETIC MODIFIERS PROMOTING OPTIC NERVE REGENERATIONR21EY029077 · NEI · WASHINGTON UNIVERSITY · PI CAVALLI, VALERIA · 2018 to 2019
$419k
Define molecular events driving selective neuronal death in multiple neurodegenerative diseases by snRNA-seqR03AG070474 · NIA · WASHINGTON UNIVERSITY · PI XU, JINBIN, ZHAO, GUOYAN · 2021 to 2022
$315k
NEI NIH HHS EY029077NEI NIH HHS R21 EY029077NIA NIH HHS R03 AG070474NIH HHS AG070474NINDS NIH HHS NS096034NINDS NIH HHS R01 NS092865NINDS NIH HHS R01 NS096034NINDS NIH HHS R01 NS123571NINDS NIH HHS R35 NS122260
6 · The paper itself

Abstract

Retinal Ganglion Cells (RGCs) lose their ability to grow axons during development. Adult RGCs thus fail to regenerate their axons after injury, leading to vision loss. To uncover mechanisms that promote regeneration of RGC axons, we identified transcription factors (TF) and open chromatin regions that are enriched in rat embryonic RGCs (high axon growth capacity) compared to postnatal RGCs (low axon growth capacity). We found that developmental stage-specific gene expression changes correlated with changes in promoter chromatin accessibility. Binding motifs for TFs such as CREB, CTCF, JUN and YY1 were enriched in the regions of the chromatin that were more accessible in embryonic RGCs. Proteomic analysis of purified rat RGC nuclei confirmed the expression of TFs with potential role in axon growth such as CREB, CTCF, YY1, and JUND. The CREB/ATF binding motif was widespread at the open chromatin region of known pro-regenerative TFs, supporting a role of CREB in regulating axon regeneration. Consistently, overexpression of CREB fused to the VP64 transactivation domain in mouse RGCs promoted axon regeneration after optic nerve injury. Our study provides a map of the chromatin accessibility during RGC development and highlights that TF associated with developmental axon growth can stimulate axon regeneration in mature RGC.

Indexed as

AnimalsAxonsChromatinCREB-Binding ProteinGene ExpressionMiceNerve RegenerationOptic NerveOptic Nerve InjuriesRatsRetinal Ganglion CellsTranscription FactorsChromatinCREB-Binding ProteinTranscription Factors

Identifiers

PMID34290335
PMCPMC8295311
OpenAlexW3185617170

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.