ArticleNeuroscience bulletin2022
Lipocalin-2-Mediated Insufficient Oligodendrocyte Progenitor Cell Remyelination for White Matter Injury After Subarachnoid Hemorrhage via SCL22A17 Receptor/Early Growth Response Protein 1 Signaling.
Article in Neuroscience bulletin, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting lipocalin-2 for multiple sclerosis: a dual role in diagnosis and therapy.Frontiers in immunology · 2026Review
- Pharmacological inhibition of SPAK-NKCC1 complex attenuates astrogliosis and restores cerebral blood flow in a mouse model of VCID.Acta neuropathologica communications · 2025Article
- Single-Cell Transcriptomics Revealed White Matter Repair Following Subarachnoid Hemorrhage.Translational stroke research · 2025Article
- Identification of pivotal genes and regulatory networks associated with SAH based on multi-omics analysis and machine learning.Scientific reports · 2025Article
- TIMP-3 Alleviates White Matter Injury After Subarachnoid Hemorrhage in Mice by Promoting Oligodendrocyte Precursor Cell Maturation.Cellular and molecular neurobiology · 2024Article
- The interaction of lipocalin-2 and astrocytes in neuroinflammation: mechanisms and therapeutic application.Frontiers in immunology · 2024Review
- Lipocalin 2 receptors: facts, fictions, and myths.Frontiers in immunology · 2023Review
- Lipid Metabolism Reprogramming of Immune Cells in Acne: An Update.Clinical, cosmetic and investigational dermatology · 2023Review
- Myelin sheath injury and repairment after subarachnoid hemorrhage.Frontiers in pharmacology · 2023Review
- White Matter Injury: An Emerging Potential Target for Treatment after Subarachnoid Hemorrhage.Oxidative medicine and cellular longevity · 2023Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insufficient remyelination due to impaired oligodendrocyte precursor cell (OPC) differentiation and maturation is strongly associated with irreversible white matter injury (WMI) and neurological deficits. We analyzed whole transcriptome expression to elucidate the potential role and underlying mechanism of action of lipocalin-2 (LCN2) in OPC differentiation and WMI and identified the receptor SCL22A17 and downstream transcription factor early growth response protein 1 (EGR1) as the key signals contributing to LCN2-mediated insufficient OPC remyelination. In LCN-knockdown and OPC EGR1 conditional-knockout mice, we discovered enhanced OPC differentiation in developing and injured white matter (WM); consistent with this, the specific inactivation of LCN2/SCl22A17/EGR1 signaling promoted remyelination and neurological recovery in both atypical, acute WMI due to subarachnoid hemorrhage and typical, chronic WMI due to multiple sclerosis. This potentially represents a novel strategy to enhance differentiation and remyelination in patients with white matter 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.