ArticleJournal of neuroinflammation2023
Inhibition of UTX/KDM6A improves recovery of spinal cord injury by attenuating BSCB permeability and macrophage infiltration through the MLCK/p-MLC pathway.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 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
- Sexual Dimorphism in Spinal Cord Injury: From Molecular Mechanisms to Clinical Translation.Neuromolecular medicine · 2026Review
- Targeted HAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Dimethyloxalylglycine improves functional recovery through inhibiting cell apoptosis and enhancing blood-spinal cord barrier repair after spinal cord injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2025Article
- Quercetin promotes angiogenesis and protects the blood-spinal cord barrier structure after spinal cord injury by targeting the PI3K/Akt signaling pathway.Journal of translational medicine · 2025Article
- UTX Responds to Nanotopography to Suppress Macrophage Inflammatory Response by Remodeling H3K27me3 Modification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Iridoids derived from Valeriana jatamansi Jones alleviates neuroinflammation and blood spinal cord barrier permeability after spinal cord injury by activating the Nrf2/HO-1 signaling pathway.Frontiers in pharmacology · 2025Article
- A transient blood IL-17 increase triggers neuroinflammation in cerebellum and motor incoordination in hyperammonemic rats.Journal of neuroinflammation · 2024Article
- Endothelial Foxo1 Phosphorylation Inhibition via Aptamer-Liposome Alleviates OPN-Induced Pathological Vascular Remodeling Following Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- MCT1-mediated endothelial cell lactate shuttle as a target for promoting axon regeneration after spinal cord injury.Theranostics · 2024Article
- Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Spinal cord injury (SCI) can prompt an immediate disruption to the blood-spinal cord barrier (BSCB). Restoring the integrity of this barrier is vital for the recovery of neurological function post-SCI. The UTX protein, a histone demethylase, has been shown in previous research to promote vascular regeneration and neurological recovery in mice with SCI. However, it is unclear whether UTX knockout could facilitate the recovery of the BSCB by reducing its permeability. In this study, we systematically studied BSCB disruption and permeability at different time points after SCI and found that conditional UTX deletion in endothelial cells (ECs) can reduce BSCB permeability, decrease inflammatory cell infiltration and ROS production, and improve neurological function recovery after SCI. Subsequently, we used RNA sequencing and ChIP-qPCR to confirm that conditional UTX knockout in ECs can down-regulate expression of myosin light chain kinase (MLCK), which specifically mediates myosin light chain (MLC) phosphorylation and is involved in actin contraction, cell retraction, and tight junctions (TJs) protein integrity. Moreover, we found that MLCK overexpression can increase the ratio of p-MLC/MLC, further break TJs, and exacerbate BSCB deterioration. Overall, our findings indicate that UTX knockout could inhibit the MLCK/p-MLC pathway, resulting in decreased BSCB permeability, and ultimately promoting neurological recovery in mice. These results suggest that UTX is a promising new target for treating SCI.
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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.