ArticleMolecular therapy : the journal of the American Society of Gene Therapy2019
UTX/KDM6A Deletion Promotes Recovery of Spinal Cord Injury by Epigenetically Regulating Vascular Regeneration.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 75 citations in OpenAlex.
- KDM6A/MMP-3 epigenetic axis governs macrophage senescence after spinal cord injury for mediating the regenerative niche to promote neurological repair.Journal of advanced research · 2026Article
- The JMJD family histone demethylases: structure, mechanism of action, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Integrative analysis identifies Hspa5 as a key regulator of the ERS/UPR-immune axis in spinal cord injury.Frontiers in genetics · 2026Article
- Deletion of the X-chromosomal geneScience translational medicine · 2025Article
- Unveiling the molecular and cellular links between obstructive sleep apnea-hypopnea syndrome and vascular aging.Chinese medical journal · 2025Review
- Overexpression of miRNA-216 in exosomes derived from umbilical cord mesenchymal stem cells promotes angiogenesis and improves functional recovery after spinal cord injury.Iranian journal of basic medical sciences · 2025Article
- UTX/Top2β axis mediated spinal cord microvascular endothelial cells senescence exacerbates spinal cord injury.PloS one · 2025Article
- Nfkbia-driven neuroinflammatory pathways mediate depression following spinal cord injury.Frontiers in molecular neuroscience · 2025Article
- Endothelial Foxo1 Phosphorylation Inhibition via Aptamer-Liposome Alleviates OPN-Induced Pathological Vascular Remodeling Following Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- miR-NPs-RVG promote spinal cord injury repair: implications from spinal cord-derived microvascular endothelial cells.Journal of nanobiotechnology · 2024Article
- Deubiquitinase UCHL1 promotes angiogenesis and blood-spinal cord barrier function recovery after spinal cord injury by stabilizing Sox17.Cellular and molecular life sciences : CMLS · 2024Article
- Local delivery of EGFRBioactive materials · 2024Article
- Epigenetic mechanism of miR-26b-5p-enriched MSCs-EVs attenuates spinal cord injury.Regenerative therapy · 2024Article
- Extracellular vesicles from UTX-knockout endothelial cells boost neural stem cell differentiation in spinal cord injury.Cell communication and signaling : CCS · 2024Article
- Curcumin can improve spinal cord injury by inhibiting DNA methylation.Molecular and cellular biochemistry · 2024Article
- Inhibition of UTX/KDM6A improves recovery of spinal cord injury by attenuating BSCB permeability and macrophage infiltration through the MLCK/p-MLC pathway.Journal of neuroinflammation · 2023Article
- Microvascular endothelial cells derived from spinal cord promote spinal cord injury repair.Bioactive materials · 2023Article
- Thermosensitive hydrogel-based GPR124 delivery strategy for rebuilding blood-spinal cord barrier.Bioengineering & translational medicine · 2023Article
- The circ_006573/miR-376b-3p Axis Advances Spinal Cord Functional Recovery after Injury by Modulating Vascular Regeneration.Molecular neurobiology · 2023Article
- UTX deletion promotes M2 macrophage polarization by epigenetically regulating endothelial cell-macrophage crosstalk after spinal cord injury.Journal of nanobiotechnology · 2023Article
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regeneration of the blood vessel system post spinal cord injury (SCI) is essential for the repair of neurological function. As a significant means to regulate gene expression, epigenetic regulation of angiogenesis in SCI is still largely unknown. Here, we found that Ubiquitously Transcribed tetratricopeptide repeat on chromosome X (UTX), the histone H3K27 demethylase, increased significantly in endothelial cells post SCI. Knockdown of UTX can promote the migration and tube formation of endothelial cells. The specific knockout of UTX in endothelial cells enhanced angiogenesis post SCI accompanied with improved neurological function. In addition, we found regulation of UTX expression can change the level of microRNA 24 (miR-24) in vitro. The physical binding of UTX to the promotor of miR-24 was indicated by chromatin immunoprecipitation (ChIP) assay. Meanwhile, methylation sequencing of endothelial cells demonstrated that UTX could significantly decrease the level of methylation in the miR-24 promotor. Furthermore, miR-24 significantly abolished the promoting effect of UTX deletion on angiogenesis in vitro and in vivo. Finally, we predicted the potential target mRNAs of miR-24 related to angiogenesis. We indicate that UTX deletion can epigenetically promote the vascular regeneration and functional recovery post SCI by forming a regulatory network with miR-24.
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