ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Lipocalin 2 plays an immunomodulatory role and has detrimental effects after spinal cord injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 123 citations in OpenAlex.
- Trial
- TIA1-mediated stress granules inhibit the neuroinflammation and neurodegeneration after spinal cord injury through LCN2 signaling.Cellular and molecular life sciences : CMLS · 2026Article
- Emerging roles of lipocalin-2-mediated neuroimmune interactions in chronic pain and itch.Frontiers in pharmacology · 2026Review
- Article
- LCN2 Regulates Microglia Polarization Through the p38MAPK-PGC-1α-PPARγ Pathway to Alleviate Traumatic Brain Injury.Cell biochemistry and biophysics · 2025Article
- The Circadian Clock Component REV-ERB Is an Analgesic Target for Cancer-Induced Tactile Pain Hypersensitivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Endoplasmic Reticulum Stress Drives Neuroinflammation Through Lipocalin 2 Upregulation in Retinal Microglia After Optic Nerve Injury.Investigative ophthalmology & visual science · 2025Article
- Upregulation of lipocalin-2 in the retina of experimental autoimmune uveitis.The Journal of veterinary medical science · 2025Article
- Sirt1 blocks nucleus pulposus and macrophages crosstalk by inhibiting RelA/Lipocalin 2 axis.Journal of orthopaedic translation · 2025Article
- Alterations in neutrophil mRNA profiles in multiple sclerosis and identification of candidate genes for further investigation.Frontiers in neurology · 2025Article
- Review
- Dexamethasone targets actin cytoskeleton signaling and inflammatory mediators to reverse sulfur mustard-induced toxicity in rabbit corneas.Toxicology and applied pharmacology · 2024Article
- Proteomics identifies lipocalin-2 in neonatal inflammation associated with cerebrovascular alteration in mice and preterm infants.iScience · 2023Article
- Interleukin-36 Receptor Signaling Attenuates Epithelial Wound Healing in C57BL/6 Mouse Corneas.Cells · 2023Article
- Lipocalin-2 Is a Key Regulator of Neuroinflammation in Secondary Traumatic and Ischemic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Reciprocal interactions between innate immune cells and astrocytes facilitate neuroinflammation and brain metastasis via lipocalin-2.Nature cancer · 2023Article
- A TRPV4-dependent neuroimmune axis in the spinal cord promotes neuropathic pain.The Journal of clinical investigation · 2023Article
- Iron homeostasis and post-hemorrhagic hydrocephalus: a review.Frontiers in neurology · 2023Review
- Serum neutrophil gelatinase-associated lipocalin as a potential biomarker for cognitive decline in spinal cord injury.Frontiers in neurology · 2023Article
- Remodeling of astrocyte secretome in amyotrophic lateral sclerosis: uncovering novel targets to combat astrocyte-mediated toxicity.Translational neurodegeneration · 2022Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Lipocalin 2 (Lcn2) plays an important role in defense against bacterial infection by interfering with bacterial iron acquisition. Although Lcn2 is expressed in a number of aseptic inflammatory conditions, its role in these conditions remains unclear. We examined the expression and role of Lcn2 after spinal cord injury (SCI) in adult mice by using a contusion injury model. Lcn2 expression at the protein level is rapidly increased 12-fold at 1 d after SCI and decreases gradually thereafter, being three times as high as control levels at 21 d after injury. Lcn2 expression is strongly induced after contusion injury in astrocytes, neurons, and neutrophils. The Lcn2 receptor (Lcn2R), which has been shown to influence cell survival, is also expressed after SCI in the same cell types. Lcn2-deficient (Lcn2⁻/⁻) mice showed significantly better locomotor recovery after spinal cord contusion injury than wild-type (Lcn2⁺/⁺) mice. Histological assessments indicate improved neuronal and tissue survival and greater sparing of myelin in Lcn2⁻/⁻ mice after contusion injury. Flow cytometry showed a decrease in neutrophil influx and a small increase in the monocyte population in Lcn2⁻/⁻ injured spinal cords. This change was accompanied by a reduction in the expression of several pro-inflammatory chemokines and cytokines as well as inducible nitric oxide synthase early after SCI in Lcn2⁻/⁻ mice compared with wild-type animals. Our results, therefore, suggest a role for Lcn2 in regulating inflammation in the injured spinal cord and that lack of Lcn2 reduces secondary damage and improves locomotor recovery after spinal cord contusion 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.