Evidence map›Paper›PMID 26077348›Full record

ArticleNature communications2015

The matricellular protein CCN1 mediates neutrophil efferocytosis in cutaneous wound healing.

Joon-Il Jun, Ki-Hyun Kim, Lester F Lau

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Low-dose ionizing radiationMaterials today. Bio · 2025
    Article
  9. Article
  10. Review
  11. Beyond Killing: The Overlooked Contribution of Neutrophils to Tissue Repair.International journal of molecular sciences · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Efferocytosis in Homeostasis.Advances in experimental medicine and biology · 2025
    Review
  16. Apoptosis and Cell Clearance in Skin Wound Healing.Advances in experimental medicine and biology · 2025
    Review
  17. Article
  18. Review
  19. Review
  20. Article

35 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Joon-Il JunDepartment of Biochemistry and Molecular Genetics, College of Medicine, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, Illinois 60607, USA.
Ki-Hyun KimDepartment of Biochemistry and Molecular Genetics, College of Medicine, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, Illinois 60607, USA.
Lester F LauDepartment of Biochemistry and Molecular Genetics, College of Medicine, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, Illinois 60607, USA.
University of Illinois Chicago · USAshland (United States) · US

Funding

Regulation of TNF-alpha by Integrin-Mediated Matrix SignalingR01GM078492 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAU, LESTER F · 2007 to 2018
$4.3M
The Matricellular Protein CCN1 in Wound HealingR01AR061791 · NIAMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAU, LESTER F · 2011 to 2021
$3.8M
NIAMS NIH HHS R01 AR061791NIAMS NIH HHS R01AR061791NIGMS NIH HHS R01 GM078492NIGMS NIH HHS R01GM78492
6 · The paper itself

Abstract

Neutrophil infiltration constitutes the first step in wound healing, although their timely clearance by macrophage engulfment, or efferocytosis, is critical for efficient tissue repair. However, the specific mechanism for neutrophil clearance in wound healing remains undefined. Here we uncover a key role for CCN1 in neutrophil efferocytosis by acting as a bridging molecule that binds phosphatidylserine, the 'eat-me' signal on apoptotic cells and integrins αvβ3/αvβ5 in macrophages to trigger efferocytosis. Both knockin mice expressing a mutant CCN1 that is unable to bind αvβ3/αvβ5 and mice with Ccn1 knockdown are defective in neutrophil efferocytosis, resulting in exuberant neutrophil accumulation and delayed healing. Treatment of wounds with CCN1 accelerates neutrophil clearance in both Ccn1 knockin mice and diabetic Lepr(db/db) mice, which suffer from neutrophil persistence and impaired healing. These findings establish CCN1 as a critical opsonin in skin injury and suggest a therapeutic potential for CCN1 in certain types of non-healing wounds.

Indexed as

AnimalsCell Migration AssaysCysteine-Rich Protein 61CytophagocytosisDiabetes MellitusEpidermal Growth FactorFluorescent Antibody TechniqueHumansImmunoprecipitationKeratinocytesMacrophagesMiceMice, Inbred C57BLNeutrophilsReal-Time Polymerase Chain ReactionReceptors, LeptinCCN1 protein, humanCCN1 protein, mouseCysteine-Rich Protein 61Epidermal Growth Factorintegrin alphaVbeta5leptin receptor, mouseReceptors, LeptinReceptors, Vitronectin

Identifiers

PMID26077348
PMCPMC4480344
OpenAlexW2254207900

What OpenQuestion holds

Textmetadata
LicenceTDM
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.