ArticlePloS one2014
CCN1 induces oncostatin M production in osteoblasts via integrin-dependent signal pathways.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- A glucocorticoid spike derails muscle repair to heterotopic ossification after spinal cord injury.Cell reports. Medicine · 2024Article
- Integrative bioinformatics analysis reveals novel insights into osteoarthritis pathogenesis and diagnostic biomarkers.BMC musculoskeletal disorders · 2024Article
- CCN1-Mediated Signaling in Placental Villous Tissues after SARS-CoV-2 Infection in Term Pregnant Women: Implications for Dysregulated Angiogenesis.Current issues in molecular biology · 2024Article
- Oncostatin M: Dual Regulator of the Skeletal and Hematopoietic Systems.Current osteoporosis reports · 2024Review
- Harmonizing hope: navigating the osteoarthritis melody through the CCL2/CCR2 axis for innovative therapeutic avenues.Frontiers in immunology · 2024Review
- Oncostatin M is a regulator of fibroblast growth factor 23 (FGF23) in UMR106 osteoblast-like cells.Scientific reports · 2023Article
- WISP-3 Stimulates VEGF-C-Dependent Lymphangiogenesis in Human Chondrosarcoma Cells by Inhibiting miR-196a-3p Synthesis.Biomedicines · 2021Article
- Visfatin Promotes the Metastatic Potential of Chondrosarcoma Cells by Stimulating AP-1-Dependent MMP-2 Production in the MAPK Pathway.International journal of molecular sciences · 2021Article
- The mir-423-5p/MMP-2 Axis Regulates the Nerve Growth Factor-Induced Promotion of Chondrosarcoma Metastasis.Cancers · 2021Article
- Targeting CCN Proteins in Rheumatoid Arthritis and Osteoarthritis.International journal of molecular sciences · 2021Review
- Conjunction junction, what's the function? CCN proteins as targets in fibrosis and cancers.American journal of physiology. Cell physiology · 2020Review
- MicroRNA-381-A Key Transcriptional Regulator: Its Biological Function and Clinical Application Prospects in Cancer.Frontiers in oncology · 2020Review
- YAP and TAZ Mediate Osteocyte Perilacunar/Canalicular Remodeling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- CCN1 stimulated the osteoblasts via PTEN/AKT/GSK3β/cyclinD1 signal pathway in Myeloma Bone Disease.Cancer medicine · 2020Article
- Oncostatin M promotes the osteogenic differentiation of mouse MC3T3‑E1osteoblasts through the regulation of monocyte chemotactic protein‑1.Molecular medicine reports · 2018Article
- Hypoxia induced mitogenic factor (HIMF) triggers angiogenesis by increasing interleukin-18 production in myoblasts.Scientific reports · 2017Article
- Enhancement of CCL2 expression and monocyte migration by CCN1 in osteoblasts through inhibiting miR-518a-5p: implication of rheumatoid arthritis therapy.Scientific reports · 2017Article
- Kuei-Lu-Er-Xian-Jiao extract enhances BMP-2 production in osteoblasts.BioMedicine · 2017Article
- Slug Modulates UV Radiation-Induced Cutaneous Inflammation by Regulating Epidermal Production of Proinflammatory Cytokines.The Journal of investigative dermatology · 2017Article
- Basic fibroblast growth factor promotes VEGF-C-dependent lymphangiogenesis via inhibition of miR-381 in human chondrosarcoma cells.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory response and articular destruction are common symptoms of osteoarthritis. Cysteine-rich 61 (CCN1 or Cyr61), a secreted protein from the CCN family, is associated with the extracellular matrix involved in many cellular activities like growth and differentiation. Yet the mechanism of CCN1 interacting with arthritic inflammatory response is unclear. This study finds CCN1 increasing expression of oncostatin m (OSM) in human osteoblastic cells. Pretreatment of αvβ3 monoclonal antibody and inhibitors of focal adhesion kinase (FAK), c-Src, phosphatidylinositol 3-kinase (PI3K), and NF-κB inhibited CCN1-induced OSM expression in osteoblastic cells. Stimulation of cells with CCN1 increased phosphorylation of FAK, c-Src, PI3K, and NF-κB via αvβ3 receptor; CCN1 treatment of osteoblasts increased NF-κB-luciferase activity and p65 binding to NF-κB element on OSM promoter. Results indicate CCN1 heightening OSM expression via αvβ3 receptor, FAK, c-Src, PI3K, and NF-κB signal pathway in osteoblastic cells, suggesting CCN1 as a novel target in arthritis treatment.
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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.