Evidence map›Paper›PMID 23836894›Full record

ArticleThe Journal of biological chemistry2013

Role of lipocalin-2-chemokine axis in the development of neuropathic pain following peripheral nerve injury.

Sangmin Jeon, Mithilesh Kumar Jha, Jiyeon Ock, Jungwan Seo, Myungwon Jin, Heejung Cho, Won-Ha Lee, Kyoungho Suk

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Glial cells in neuropathic pain.Physiological reviews · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. 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 · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Differential Gene Expression in Pain-Related Genes are not Affected by the Presence of Dementia.Pain management nursing : official journal of the American Society of Pain Management Nurses · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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 · 2023
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Sangmin JeonDepartment of Pharmacology, Brain Science and Engineering Institute, Kyungpook National University School of Medicine, Daegu 700-422, Korea.
Mithilesh Kumar Jha
Jiyeon Ock
Jungwan Seo
Myungwon Jin
Heejung Cho
Won-Ha Lee
Kyoungho Suk
Kyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipocalin 2 (LCN2), which is also known as 24p3 and neutrophil gelatinase-associated lipocalin (NGAL), binds small, hydrophobic ligands and interacts with cell surface receptor 24p3R to regulate diverse cellular processes. In the present study, we examined the role of LCN2 in the pathogenesis of neuropathic pain using a mouse model of spared nerve injury (SNI). Lcn2 mRNA levels were significantly increased in the dorsal horn of the spinal cord after SNI, and LCN2 protein was mainly localized in neurons of the dorsal and ventral horns. LCN2 receptor 24p3R was expressed in spinal neurons and microglia after SNI. Lcn2-deficient mice exhibited significantly less mechanical pain hypersensitivity during the early phase after SNI, and an intrathecal injection of recombinant LCN2 protein elicited mechanical pain hypersensitivity in naive animals. Lcn2 deficiency, however, did not affect acute nociceptive pain. Lcn2-deficient mice showed significantly less microglial activation and proalgesic chemokine (CCL2 and CXCL1) production in the spinal cord after SNI than wild-type mice, and recombinant LCN2 protein induced the expression of these chemokines in cultured neurons. Furthermore, the expression of LCN2 and its receptor was detected in neutrophils and macrophages in the sciatic nerve following SNI, suggesting the potential role of peripheral LCN2 in neuropathic pain. Taken together, our results indicate that LCN2 plays a critical role in the development of pain hypersensitivity following peripheral nerve injury and suggest that LCN2 mediates neuropathic pain by inducing chemokine expression and subsequent microglial activation.

Indexed as

Signal TransductionAcute-Phase ProteinsAnimalsCells, CulturedCerebral CortexChemokinesGene Expression RegulationHyperalgesiaLipocalin-2LipocalinsMiceMice, Inbred C57BLMicrogliaModels, BiologicalNeuralgiaNeuronsAcute-Phase ProteinsChemokinesLcn2 protein, mouseLipocalin-2LipocalinsOncogene Proteinsp38 Mitogen-Activated Protein KinasesReceptors, Cell SurfaceRNA, MessengerSlc22a17 protein, mouseChemokinesGliaNerveNeuroinflammationNeuropathic PainPainSpinal Cord

Identifiers

PMID23836894
PMCPMC3745354
OpenAlexW2043599256

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.