The matricellular protein CCN1 mediates neutrophil efferocytosis in cutaneous wound healing
Open accessAbstract
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 Leprdb/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. Neutrophils are the first line of response to injury but their persistence can inhibit the resolution phase of tissue repair. Here the authors show that an extracellular matrix protein promotes neutrophil clearance by macrophages, serving as a bridge between the two cell types and speeding up tissue repair.
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CCN1 is released from activated platelets and macrophages and can mediate signals from injuries and hemostasis.
“CCN1 is released from activated platelets and macrophages (62, 63) and thus can mediate signals from injuries and hemostasis.”
From Senescent hepatic stellate cells promote liver regeneration through IL-6 and ligands of CXCR2 (2022) · cites this paper as [63]
The Discussion (page unavailable) says CCN1 is expressed in macrophages and may be secreted by diverse cell types in the wound microenvironment. It does not establish that activated platelets release CCN1; the Introduction mentions platelet-associated clotting but does not identify CCN1 as a platelet-released factor. The proposed link to hemostasis is therefore not established by this paper. (LLM, conf=0.82)
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- Authors
- Jun, J.-I., Kim, K.-H., & Lau, L. F.
- Affiliations
- University of Illinois Chicago (US)
- Corresponding author
- Lau, Lester F.
- ORCID
- Lau, Lester F.
- Venue
- Nature Communications
- Published
- 2015-06-16
- Volume
- 6
- Issue
- 1
- Pages
- 7386-7386
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4480344
- OpenAlex
- W2254207900
- Cited by
- 173
- References
- 74
- Citations by year
- 2026: 7 · 2025: 19 · 2024: 16 · 2023: 14 · 2022: 24 · 2021: 15 · 2020: 17 · 2019: 17 · 2018: 14 · 2017: 15 · 2016: 13 · 2015: 2
- FWCI
- 14.81
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (R01GM078492, R01-GM78492)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR061791)
- Topics
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- CYR61, skin wound healing, phosphatidylserine, integrin αvβ3, integrin αvβ5, macrophages, neutrophil clearance, opsonins, extracellular matrix proteins, diabetic wound healing, inflammation resolution
- MeSH terms
- Animals, Diabetes Mellitus, Epidermal Growth Factor, Fluorescent Antibody Technique, Humans, Macrophages, Mice, Inbred C57BL, Neutrophils, Skin, Wound Healing, Keratinocytes, Receptors, Vitronectin, Reverse Transcriptase Polymerase Chain Reaction, Immunoprecipitation, Mice, Receptors, Leptin, Cell Migration Assays, Cysteine-Rich Protein 61, Cytophagocytosis, Real-Time Polymerase Chain Reaction
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