ArticleThe Journal of biological chemistry2015
Dynamic regulation of Schwann cell enhancers after peripheral nerve injury.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 123 citations in OpenAlex.
- Long-term ocular symptoms following COVID-19 linked to immune dysregulation, dysautonomia and peripheral neuropathy.Nature communications · 2026Article
- Sonic Hedgehog Agonists Induce Repair Schwann Cells.Biotechnology and bioengineering · 2025Article
- Runx2 downregulates Lpl expression through super-silencer formation to alter lipid metabolism in Zhu Schwann cells after nerve injury.Cellular & molecular biology letters · 2025Article
- Sequential activation of transcription factors promotes liver regeneration through specific and developmental enhancers.Cell genomics · 2025Article
- Article
- Runx2 drives Schwann cells repair phenotype switch through chromatin remodeling and Sox2 activation after nerve injury.Molecular medicine (Cambridge, Mass.) · 2025Article
- Dynamically changing extracellular matrix stiffness drives Schwann cell phenotype.Matrix biology plus · 2025Article
- Enhancer-driven Shh signaling promotes glia-to-mesenchyme transition during bone repair.Bone research · 2025Article
- NetREm: Network Regression Embeddings reveal cell-type transcription factor coordination for gene regulation.Bioinformatics advances · 2025Article
- Article
- TFEB/3 Govern Repair Schwann Cell Generation and Function Following Peripheral Nerve Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- A screen for regeneration-associated silencer regulatory elements in zebrafish.Developmental cell · 2024Article
- BDNF and Krox20 as Indicators of Platelet-rich Plasma-Induced Nerve Regeneration in a Neuropathic Orofacial Pain Model.European journal of dentistry · 2024Article
- Epigenetic reprogramming shapes the cellular landscape of schwannoma.Nature communications · 2024Article
- Sustainable Release Selenium Laden with SiOInternational journal of nanomedicine · 2024Article
- Local Administration of Minocycline Improves Nerve Regeneration in Two Rat Nerve Injury Models.International journal of molecular sciences · 2023Article
- Regulation of chromatin organization during animal regeneration.Cell regeneration (London, England) · 2023Review
- Article
- Epigenetic and epitranscriptomic regulation of axon regeneration.Molecular psychiatry · 2023Review
- Models and methods to study Schwann cells.Journal of anatomy · 2022Review
16 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Myelination of the peripheral nervous system is required for axonal function and long term stability. After peripheral nerve injury, Schwann cells transition from axon myelination to a demyelinated state that supports neuronal survival and ultimately remyelination of axons. Reprogramming of gene expression patterns during development and injury responses is shaped by the actions of distal regulatory elements that integrate the actions of multiple transcription factors. We used ChIP-seq to measure changes in histone H3K27 acetylation, a mark of active enhancers, to identify enhancers in myelinating rat peripheral nerve and their dynamics after demyelinating nerve injury. Analysis of injury-induced enhancers identified enriched motifs for c-Jun, a transcription factor required for Schwann cells to support nerve regeneration. We identify a c-Jun-bound enhancer in the gene for Runx2, a transcription factor induced after nerve injury, and we show that Runx2 is required for activation of other induced genes. In contrast, enhancers that lose H3K27ac after nerve injury are enriched for binding sites of the Sox10 and early growth response 2 (Egr2/Krox20) transcription factors, which are critical determinants of Schwann cell differentiation. Egr2 expression is lost after nerve injury, and many Egr2-binding sites lose H3K27ac after nerve injury. However, the majority of Egr2-bound enhancers retain H3K27ac, indicating that other transcription factors maintain active enhancer status after nerve injury. The global epigenomic changes in H3K27ac deposition pinpoint dynamic changes in enhancers that mediate the effects of transcription factors that control Schwann cell myelination and peripheral nervous system responses to nerve injury.
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Registered trials
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.