ArticleCellular and molecular life sciences : CMLS2024
Deubiquitinase UCHL1 promotes angiogenesis and blood-spinal cord barrier function recovery after spinal cord injury by stabilizing Sox17.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 20 citations in OpenAlex.
- Tissue engineering for traumatic spinal cord injury: Research advances and clinical translation.Bioactive materials · 2026Review
- UCHL1-mediated deubiquitination of PARK7 suppresses ferroptosis and enhances tumor progression in triple-negative breast cancer.Molecular and cellular biochemistry · 2026Article
- Photobiomodulation repairs the blood-spinal cord barrier in a mouse model of spinal cord injury.Neural regeneration research · 2026Article
- Single-cell RNA sequencing of the post-spinal cord injury dorsal root ganglia in cynomolgus monkeys: Elucidation of the cellular immune microenvironment of the central nervous system.Neural regeneration research · 2026Article
- Microglia-vascular interactions after spinal cord injury: regulatory mechanisms and therapeutic advances.Frontiers in immunology · 2026Review
- Article
- Deubiquitinating enzymes at the crossroads of blood-brain barrier integrity and neurodegeneration: mechanistic insights, therapeutic targeting and future directions.Tissue barriers · 2026Review
- Athlete-derived extracellular vesicles protect against spinal cord injury via inhibition of neuronal ferroptosis.Science advances · 2025Article
- Biomaterial-Based Emergency Intervention for Secondary Spinal Cord Injury.Small science · 2025Review
- UCH-L1 in Alzheimer's Disease: A Crucial Player in Dementia-Associated Mechanisms.International journal of molecular sciences · 2025Review
- Multidimensional Engineering of Extracellular Vesicles for Targeted Delivery and Microglial Reprograming in Spinal Cord Injury Repair.ACS nano · 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
- UCHL1-Mediated Spastin Degradation Regulates Microtubule Severing and Hippocampal Neurite Outgrowth.Journal of molecular neuroscience : MN · 2025Article
- Article
- Exploring Ubiquitination in Spinal Cord Injury Therapy: Multifaceted Targets and Promising Strategies.Neurochemical research · 2025Review
- Blood-spinal cord barrier alterations in a mouse model of centrifugation-induced hypergravity.Frontiers in physiology · 2025Article
- Bone marrow mesenchymal stem cells modulate miR-202-3p to suppress neuronal apoptosis following spinal cord injury through autophagy activation via the AMPK, MAPK, and PI3K/AKT/mTOR signaling pathway.Scientific reports · 2024Article
- SOX17 expression in ovarian clear cell carcinoma.Journal of ovarian research · 2024Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Improving the function of the blood-spinal cord barrier (BSCB) benefits the functional recovery of mice following spinal cord injury (SCI). The death of endothelial cells and disruption of the BSCB at the injury site contribute to secondary damage, and the ubiquitin-proteasome system is involved in regulating protein function. However, little is known about the regulation of deubiquitinated enzymes in endothelial cells and their effect on BSCB function after SCI. We observed that Sox17 is predominantly localized in endothelial cells and is significantly upregulated after SCI and in LPS-treated brain microvascular endothelial cells. In vitro Sox17 knockdown attenuated endothelial cell proliferation, migration, and tube formation, while in vivo Sox17 knockdown inhibited endothelial regeneration and barrier recovery, leading to poor functional recovery after SCI. Conversely, in vivo overexpression of Sox17 promoted angiogenesis and functional recovery after injury. Additionally, immunoprecipitation-mass spectrometry revealed the interaction between the deubiquitinase UCHL1 and Sox17, which stabilized Sox17 and influenced angiogenesis and BSCB repair following injury. By generating UCHL1 conditional knockout mice and conducting rescue experiments, we further validated that the deubiquitinase UCHL1 promotes angiogenesis and restoration of BSCB function after injury by stabilizing Sox17. Collectively, our findings present a novel therapeutic target for treating SCI by revealing a potential mechanism for endothelial cell regeneration and BSCB repair after 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.