ArticleOsteoarthritis and cartilage2015
Function of the chondrocyte PI-3 kinase-Akt signaling pathway is stimulus dependent.
Article in Osteoarthritis and cartilage, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Response eQTLs, chromatin accessibility, and 3D chromatin structure in chondrocytes provide mechanistic insight into osteoarthritis risk.Cell genomics · 2025Article
- Response eQTLs, chromatin accessibility, and 3D chromatin structure in chondrocytes provide mechanistic insight into osteoarthritis risk.bioRxiv : the preprint server for biology · 2024Article
- Dysregulated Genes and Signaling Pathways in the Formation and Rupture of Intracranial Aneurysm.Translational stroke research · 2024Article
- Natural products in osteoarthritis treatment: bridging basic research to clinical applications.Chinese medicine · 2024Review
- Revealing a Natural Model of Pre-Osteoarthritis of the Hip Through Study of Femoroacetabular Impingement.HSS journal : the musculoskeletal journal of Hospital for Special Surgery · 2023Article
- Vanillin-based functionalization strategy to construct multifunctional microspheres for treating inflammation and regenerating intervertebral disc.Bioactive materials · 2023Article
- Vaspin promotes chondrogenic differentiation of BMSCs via Akt activation in osteoarthritis.BMC musculoskeletal disorders · 2022Article
- Madecassic Acid Ameliorates the Progression of Osteoarthritis: An in vitro and in vivo Study.Drug design, development and therapy · 2022Article
- Hype or hope of hyaluronic acid for osteoarthritis: Integrated clinical evidence synthesis with multi-organ transcriptomics.Journal of orthopaedic translation · 2022Article
- Adipose-Derived Extract Suppresses IL-1β-Induced Inflammatory Signaling Pathways in Human Chondrocytes and Ameliorates the Cartilage Destruction of Experimental Osteoarthritis in Rats.International journal of molecular sciences · 2021Article
- Chondrocyte Aging: The Molecular Determinants and Therapeutic Opportunities.Frontiers in cell and developmental biology · 2021Review
- Deletion of JNK Enhances Senescence in Joint Tissues and Increases the Severity of Age-Related Osteoarthritis in Mice.Arthritis & rheumatology (Hoboken, N.J.) · 2020Article
- Anti-Inflammatory and Chondroprotective Effects of Vanillic Acid and Epimedin C in Human Osteoarthritic Chondrocytes.Biomolecules · 2020Article
- Article
- Loganin Attenuates Osteoarthritis in Rats by Inhibiting IL-1β-Induced Catabolism and Apoptosis in Chondrocytes Via Regulation of Phosphatidylinositol 3-Kinases (PI3K)/Akt.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- TGF-β type 2 receptor-mediated modulation of the IL-36 family can be therapeutically targeted in osteoarthritis.Science translational medicine · 2019Article
- Articular chondrocytes isolated from the knee and ankle joints of human tissue donors demonstrate similar redox-regulated MAP kinase and Akt signaling.Osteoarthritis and cartilage · 2019Article
- Differential peroxiredoxin hyperoxidation regulates MAP kinase signaling in human articular chondrocytes.Free radical biology & medicine · 2019Article
- Sustained Akt signaling in articular chondrocytes causes osteoarthritis via oxidative stress-induced senescence in mice.Bone research · 2019Article
- Fetal articular cartilage regeneration versus adult fibrocartilaginous repair: secretome proteomics unravels molecular mechanisms in an ovine model.Disease models & mechanisms · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe PI-3 kinase-Akt pathway plays a role in cartilage anabolic as well as catabolic processes in response to activation by insulin-like growth factor-1 (IGF-1) and the pro-inflammatory cytokines interleukin-1β (IL-1β) and oncostatin M (OSM). The goal of this study was to determine how PI-3 kinase-Akt signaling regulates these seemingly opposing functions.
designMonolayer cultures of primary human articular chondrocytes were treated with IGF-1, IL-1β, OSM, or the combination of IL-1β and OSM in time course experiments. Activation of signaling proteins and MMP production were measured by immunoblotting. Cells were pre-treated with chemical inhibitors to block mitogen activated protein (MAP) kinases, PI-3 kinase, or JAK/STAT pathway activation. Constitutively active Akt1 and Akt3 were expressed to study stimulus-independent activation of Akt.
resultsIGF-1, OSM, and the combination of IL-1β and OSM but not IL-1β alone, stimulated phosphorylation of Akt which was sustained longer with IGF-1. IL-1β plus OSM, but not IGF-1, increased chondrocyte MMP-13 production which was inhibited with either a general PI-3 kinase inhibitor or specific inhibition of the PI-3 kinase-γ isoform. Akt1 or Akt3 activity alone was not sufficient to increase production of MMP-13. IL-1β/OSM induced MMP-13 production required activation of the MAP kinases, JNK and p38, as well as the JAK-STAT pathway which were activated by IL-1β plus OSM but not by IGF-1.
conclusionsThe chondrocyte integrates signals from the PI-3 kinase-Akt pathway with signals from MAP kinases and the JAK-STAT pathway to allow for a differential response to a pro-anabolic (IGF-1) and a pro-catabolic (IL-1β plus OSM) stimulus.
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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 Socratic graph.