ArticleThe American journal of pathology2006
p21Cip1 is required for the development of monocytes and their response to serum transfer-induced arthritis.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Key Role of STAT3 in Osteoarthritis: From Pathogenic Mechanisms to Targeted Therapy.International journal of nanomedicine · 2025Review
- Stromal and therapy-induced macrophage proliferation promotes PDAC progression and susceptibility to innate immunotherapy.The Journal of experimental medicine · 2023Article
- MCTR3 reprograms arthritic monocytes to upregulate Arginase-1 and exert pro-resolving and tissue-protective functions in experimental arthritis.EBioMedicine · 2022Article
- VISTA: A Target to Manage the Innate Cytokine Storm.Frontiers in immunology · 2020Review
- Association of Increased F4/80Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- Genetic deficiency of Wnt5a diminishes disease severity in a murine model of rheumatoid arthritis.Arthritis research & therapy · 2017Article
- Deletion of calponin 2 in macrophages attenuates the severity of inflammatory arthritis in mice.American journal of physiology. Cell physiology · 2016Article
- p21 deficiency is susceptible to osteoarthritis through STAT3 phosphorylation.Arthritis research & therapy · 2015Article
- Fas signaling in macrophages promotes chronicity in K/BxN serum-induced arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- High-resolution magnetic resonance imaging of ankle joints in murine arthritis discriminates inflammation and bone destruction in a quantifiable manner.Arthritis and rheumatism · 2013Article
- TLR2 deletion promotes arthritis through reduction of IL-10.Journal of leukocyte biology · 2013Article
- Development of a new humanized mouse model to study acute inflammatory arthritis.Journal of translational medicine · 2012Article
- Cyclin-dependent kinase inhibitor p21, via its C-terminal domain, is essential for resolution of murine inflammatory arthritis.Arthritis and rheumatism · 2012Article
- NUR who? An orphan transcription factor holds promise for monomaniacs.Nature immunology · 2011Article
- Development of monocytes, macrophages, and dendritic cells.Science (New York, N.Y.) · 2010Review
- Bim-Bcl-2 homology 3 mimetic therapy is effective at suppressing inflammatory arthritis through the activation of myeloid cell apoptosis.Arthritis and rheumatism · 2010Article
- Modulation of expression and cellular distribution of p21 by macrophage migration inhibitory factor.Journal of inflammation (London, England) · 2009Article
- Regulation of monocytes and macrophages cell fate.Frontiers in bioscience (Landmark edition) · 2009Review
- Disruption of p21 attenuates lung inflammation induced by cigarette smoke, LPS, and fMLP in mice.American journal of respiratory cell and molecular biology · 2008Article
- p21Cip1 modulates arterial wound repair through the stromal cell-derived factor-1/CXCR4 axis in mice.The Journal of clinical investigation · 2008Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
One of the central functions of cyclin-dependent kinase inhibitors, such as p21, p27, or p16, is to prevent entry into the cell cycle. However, the question remains as to whether they have other functions in the cell. We previously demonstrated that overexpression of p21 in fibroblasts isolated from patients with rheumatoid arthritis decreases the production of pro-inflammatory molecules. Overexpression of p21 has been also shown to reduce the development of experimental arthritis in mice and rats. To explore the role of endogenous p21 in the development of arthritis, we induced arthritis in p21(-/-) mice using the K/BxN serum transfer model of arthritis. Mice deficient in p21 were more resistant to serum transfer-induced arthritis (K/BxN) than wild-type (wt) control mice. Fewer macrophages were detected in p21(-/-) as compared to wt joints following transfer of K/BxN serum. Chemotaxis assays of bone marrow-derived macrophages from p21(-/-) and wt mice revealed no difference in migration. However, there was a substantial decrease in inflammatory monocytes circulating in peripheral blood and in monocyte precursors in bone marrow of p21(-/-) mice as compared to wt mice. Adoptive transfer of wt bone marrow-derived macrophages into p21(-/-) mice restored the sensitivity to serum transfer-induced arthritis. These data suggest a novel role for p21 in regulating the development and/or differentiation of monocytic populations that are crucial for the induction of inflammatory arthritis.
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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.