ArticleArthritis research & therapy2007
Src kinase inhibition promotes the chondrocyte phenotype.
Article in Arthritis research & therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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.
Who cites it
18 citing papers in PubMed, 45 citations in OpenAlex.
- Comparative efficacy of transdermal buprenorphine versus diclofenac in the management of knee osteoarthritis: a randomized controlled trial with network pharmacology insights.Inflammopharmacology · 2026Trial
- Role of external forces in the mechanobiology of stem and differentiated chondrogenic cells embedded in a tissue-engineered construct for cartilage repair.Journal of biomedical science · 2026Review
- Podocalyxin and ciliary neurotrophic factor receptor are novel components of the surfaceome of chondrogenic cells.Cell communication and signaling : CCS · 2025Article
- Hck promotes IL-1β-induced extracellular matrix degradation, inflammation, and apoptosis in osteoarthritis via activation of the JAK-STAT3 signaling pathway.Advances in rheumatology (London, England) · 2024Article
- Mechanism of icariin for the treatment of osteoarthritis based on network pharmacology and molecular docking method.American journal of translational research · 2023Article
- Enhanced differentiation of human pluripotent stem cells into pancreatic endocrine cells in 3D culture by inhibition of focal adhesion kinase.Stem cell research & therapy · 2020Article
- Actin reduction by MsrB2 is a key component of the cytokinetic abscission checkpoint and prevents tetraploidy.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Cyclic Tensile Strain Upregulates Pro-Inflammatory Cytokine Expression Via FAK-MAPK Signaling in Chondrocytes.Inflammation · 2018Article
- miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development.Developmental biology · 2017Article
- Subcellular domain-dependent molecular hierarchy of SFK and FAK in mechanotransduction and cytokine signaling.Scientific reports · 2017Article
- Distinctive subcellular inhibition of cytokine-induced SRC by salubrinal and fluid flow.PloS one · 2014Article
- Article
- Inhibitors of Src and focal adhesion kinase promote endocrine specification: impact on the derivation of β-cells from human pluripotent stem cells.The Journal of biological chemistry · 2011Article
- Cartilage biology in osteoarthritis--lessons from developmental biology.Nature reviews. Rheumatology · 2011Review
- Human stanniocalcin-1 or -2 expressed in mice reduces bone size and severely inhibits cranial intramembranous bone growth.Transgenic research · 2010Article
- Control of chondrocyte gene expression by actin dynamics: a novel role of cholesterol/Ror-alpha signalling in endochondral bone growth.Journal of cellular and molecular medicine · 2009Article
- Cartilage homeostasis in health and rheumatic diseases.Arthritis research & therapy · 2009Review
- Rho-ROCK signaling differentially regulates chondrocyte spreading on fibronectin and bone sialoprotein.American journal of physiology. Cell physiology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulated differentiation of chondrocytes is essential for both normal skeletal development and maintenance of articular cartilage. The intracellular pathways that control these events are incompletely understood, and our ability to modulate the chondrocyte phenotype in vivo or in vitro is therefore limited. Here we examine the role played by one prominent group of intracellular signalling proteins, the Src family kinases, in regulating the chondrocyte phenotype. We show that the Src family kinase Lyn exhibits a dynamic expression pattern in the chondrogenic cell line ATDC5 and in a mixed population of embryonic mouse chondrocytes in high-density monolayer culture. Inhibition of Src kinase activity using the pharmacological compound PP2 (4-Amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo [3,4-d]pyrimidine) strongly reduced the number of primary mouse chondrocytes. In parallel, PP2 treatment increased the expression of both early markers (such as Sox9, collagen type II, aggrecan and xylosyltransferases) and late markers (collagen type X, Indian hedgehog and p57) markers of chondrocyte differentiation. Interestingly, PP2 repressed the expression of the Src family members Lyn, Frk and Hck. It also reversed morphological de-differentiation of chondrocytes in monolayer culture and induced rounding of chondrocytes, and reduced stress fibre formation and focal adhesion kinase phosphorylation. We conclude that the Src kinase inhibitor PP2 promotes chondrogenic gene expression and morphology in monolayer culture. Strategies to block Src activity might therefore be useful both in tissue engineering of cartilage and in the maintenance of the chondrocyte phenotype in diseases such as osteoarthritis.
Indexed as
Identifiers
What OpenQuestion holds
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.