Vav/Phospholipase Cγ2–mediated control of a neutrophil‐dependent murine model of rheumatoid arthritis
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OBJECTIVE: Accumulating evidence indicates an important role of neutrophils in the development of rheumatoid arthritis (RA). Recruitment of neutrophils to the joint space and release of proteolytic enzymes can exacerbate tissue damage and the inflammatory response related to RA. Engagement of beta2 integrin and subsequent activation of downstream signaling have been shown to be fundamental for activation of neutrophil effector functions. The aim of this study was to test the hypothesis that Vav and phospholipase Cgamma2 (PLCgamma2), two molecules involved in integrin signaling, are required for arthritis generation and neutrophil activation in a mouse model of arthritis. METHODS: Arthritis was induced in wild-type (WT), Vav(null), and PLCgamma2(-/-) mice using the K/BxN serum-transfer model. Neutrophil function was assessed by analyses of adhesion, spreading, and degranulation on integrin-dependent substrates. Regulation of integrin signaling was determined by analyzing the phosphorylation of Pyk-2, Src, and ERK. RESULTS: Vav(null) and PLCgamma2(-/-) mice were protected from inflammation and bone erosion in the K/BxN serum-transfer model of arthritis. Mechanistically, Vav and PLCgamma2 control neutrophils mediated spreading and degranulation on integrin-dependent substrates. Consequently, the Vav/PLCgamma2 axis, acting downstream of the integrin receptor, modulated the activation of Pyk-2, Src, and ERK. CONCLUSION: Our findings show that Vav cooperates with PLCgamma2 in modulating neutrophil activation downstream of the integrin receptor. This study identifies a Vav/PLCgamma2-dependent signaling pathway as a possible therapeutic target for the treatment of inflammation and bone disruption in arthritis.
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The involvement of PLCγ2 in the K/BxN model was downstream of integrin stimulation and neutrophil activation, including neutrophil spreading and degranulation.
“This involvement of PLCγ2 was downstream of integrin stimulation and neutrophil activation, including their spreading and degranulation (112).”
From The role of PLCγ2 in immunological disorders, cancer, and neurodegeneration (2021) · cites this paper as [112]
In a K/BxN serum-transfer murine model of RA, Vav/PLCγ2-deficient mice were protected from inflammation and bone erosion.
“In a K/BxN serum-transfer murine model of RA, Vav/PLCγ2-deficient mice were protected from inflammation and bone erosion (73, 112).”
From The role of PLCγ2 in immunological disorders, cancer, and neurodegeneration (2021) · cites this paper as [112]
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Decker, C. E., Hesker, P. R., Zhang, K., & Faccio, R. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m113.477281 · Cited by 9 · see citing works
Self-citationRevisit of autoimmunity to glucose-6-phosphate isomerase in experimental and rheumatoid arthritis
Matsumoto, I., Kurata, I., Ohyama, A., Kawaguchi, H., Ebe, H., Osada, A., Kondo, Y., Tsuboi, H., & Sumida, T. (2019) · Modern Rheumatology · doi:10.1080/14397595.2019.1659539 · Cited by 8 · see citing works
Phospholipase C-γ as a Potential Therapeutic Target for Graves’ Orbitopathy
Roh, T. H., Chae, M. K., Ko, J., Kikkawa, D. O., Jang, S. Y., & Yoon, J. S. (2023) · Endocrinology and Metabolism · doi:10.3803/enm.2023.1780 · Cited by 7 · see citing works
Fluorogenic XY-69 in Lipid Vesicles for Measuring Activity of Phospholipase C Isozymes
Carr, A. J., Siraliev-Perez, E., Huang, W., Sondek, J., & Zhang, Q. (2021) · Methods in molecular biology · doi:10.1007/978-1-0716-1142-5_17 · Cited by 7 · see citing works
Unravelling the roles of Vav3 in cytoskeletal control and angiogenesis
Wang, Y., Wang, Z., Diao, W., Shi, T., Xu, J., Deng, T., Wen, C., Gu, J., Deng, T., & Xiao, C. (2025) · Life Sciences · doi:10.1016/j.lfs.2025.123834 · Cited by 6 · see citing works
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Self-citationDistinct Roles of Vav Family Members in Adaptive and Innate Immune Models of Arthritis
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Phospo-PKCs in Abeta1-42-Specific Human T Cells from Alzheimer’s Disease Patients
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Phospholipase C Isoform Functions in Immune Cells
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- Authors
- Cremasco, V., Graham, D. B., Novack, D. V., Swat, W., & Faccio, R.
- Affiliations
- Washington University in St. Louis (US)
- Venue
- Arthritis & Rheumatism
- Publisher
- Wiley
- Published
- 2008-08-29
- Volume
- 58
- Issue
- 9
- Pages
- 2712-2722
- ISSN
- 0004-3591 (ISSN-L)
- 1529-0131
- PMC
- PMC3004987
- OpenAlex
- W2083433555
- Cited by
- 51
- References
- 49
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 5 · 2020: 2 · 2019: 3 · 2018: 1 · 2017: 3 · 2016: 5 · 2015: 5 · 2014: 2 · 2013: 5 · 2012: 1
- FWCI
- 3.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Arthritis & Rheumatism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (T32CA009547)
- National Institute of Allergy and Infectious Diseases (AI 063024-02, R01AI061077, R21AI063024, AI-06107703)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR053628, R01-AR52921)
- Topics
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Health Sciences › Medicine › Complementary and alternative medicine › Natural Compounds in Disease Treatment
- Keywords
- rheumatoid arthritis, neutrophils, Vav, PLCγ2, K/BxN serum transfer arthritis, neutrophil degranulation, neutrophil spreading, Src kinase, ERK, bone erosion, integrin-mediated adhesion, therapeutic target
- MeSH terms
- Animals, Arthritis, Rheumatoid, Cell Adhesion, Cell Movement, Disease Models, Animal, Inflammation, Neutrophils, Phosphorylation, RNA, Messenger, Blotting, Western, Signal Transduction, Integrins, Cytokines, Mice, Knockout, Neutrophil Activation, Reverse Transcriptase Polymerase Chain Reaction, Mice, Proto-Oncogene Proteins c-vav, Phospholipase C gamma
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