ArticleMolecular & cellular proteomics : MCP2009
Mechanical injury and cytokines cause loss of cartilage integrity and upregulate proteins associated with catabolism, immunity, inflammation, and repair.
Article in Molecular & cellular proteomics : MCP, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
What it found
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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
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- An Evidence-Based Systematic Review of Human Knee Post-Traumatic Osteoarthritis (PTOA): Timeline of Clinical Presentation and Disease Markers, Comparison of Knee Joint PTOA Models and Early Disease Implications.International journal of molecular sciences · 2021Pooled it
- Motion as Medicine: Physical Activity, Joint Sensitivity, and Pain Management-A Narrative Review.Medical sciences (Basel, Switzerland) · 2026Review
- Design Strategies to Target Joint Resident Mesenchymal Stem Cells for Osteochondral Regeneration.Cells · 2026Review
- Resolving curling and swelling in cartilage and other deformation-prone tissue explant models: a scalable, simple load-predictive flattening method enabling standardized mechanical compression.Frontiers in bioengineering and biotechnology · 2026Article
- The Effect of IL-17A and Combined Mechanical Injury on Meniscal Tissue Integrity In Vitro.Journal of clinical medicine · 2025Article
- Loss of collagen content is localized near cartilage lesions on the day of injurious loading and intensified on day 12.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Advancing Osteoarthritis Research: Insights from Rodent Models and Emerging Trends.Journal of orthopaedics and sports medicine · 2025Article
- Three decades of advancements in osteoarthritis research: insights from transcriptomic, proteomic, and metabolomic studies.Osteoarthritis and cartilage · 2024Review
- A programmable arthritis-specific receptor for guided articular cartilage regenerative medicine.bioRxiv : the preprint server for biology · 2024Article
- Mechanical Articular Cartilage Injury Models and Their Relevance in Advancing Therapeutic Strategies.Advances in experimental medicine and biology · 2023Article
- In Vitro Models and Proteomics in Osteoarthritis Research.Advances in experimental medicine and biology · 2023Review
- Cell morphology as a biological fingerprint of chondrocyte phenotype in control and inflammatory conditions.Frontiers in immunology · 2023Article
- Shear strain and inflammation-induced fixed charge density loss in the knee joint cartilage following ACL injury and reconstruction: A computational study.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022Article
- The protective effect of mangiferin on osteoarthritis: An in vitro and in vivo study.Physiological research · 2022Article
- A High-Throughput Mechanical Activator for Cartilage Engineering Enables Rapid Screening of in vitro Response of Tissue Models to Physiological and Supra-Physiological Loads.Cells, tissues, organs · 2022Article
- Hyperosmolar Ionic Solutions Modulate Inflammatory Phenotype and sGAG Loss in a Cartilage Explant Model.Cartilage · 2021Article
- An Anterior Cruciate Ligament Rupture Increases Levels of Urine N-terminal Cross-linked Telopeptide of Type I Collagen, Urine C-terminal Cross-linked Telopeptide of Type II Collagen, Serum Aggrecan ARGS Neoepitope, and Serum Tumor Necrosis Factor-α.The American journal of sports medicine · 2021Article
- Inflammatory signaling sensitizes Piezo1 mechanotransduction in articular chondrocytes as a pathogenic feed-forward mechanism in osteoarthritis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- Mechanobiological model for simulation of injured cartilage degradation via pro-inflammatory cytokines and mechanical stimulus.PLoS computational biology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The objectives of this study were to perform a quantitative comparison of proteins released from cartilage explants in response to treatment with IL-1beta, TNF-alpha, or mechanical compression injury in vitro and to interpret this release in the context of anabolic-catabolic shifts known to occur in cartilage in response to these insults in vitro and their implications in vivo. Bovine calf cartilage explants from 6-12 animals were subjected to injurious compression, TNF-alpha (100 ng/ml), IL-1beta (10 ng/ml), or no treatment and cultured for 5 days in equal volumes of medium. The pooled medium from each of these four conditions was labeled with one of four iTRAQ labels and subjected to nano-2D-LC/MS/MS on a quadrupole time-of-flight instrument. Data were analysed by ProQuant for peptide identification and quantitation. k-means clustering and biological pathways analysis were used to identify proteins that may correlate with known cartilage phenotypic responses to such treatments. IL-1beta and TNF-alpha treatment caused a decrease in the synthesis of collagen subunits (p < 0.05) as well as increased release of aggrecan G2 and G3 domains to the medium (p < 0.05). MMP-1, MMP-3, MMP-9, and MMP-13 were significantly increased by all treatments compared with untreated samples (p < 0.10). Increased release of proteins involved in innate immunity and immune cell recruitment were noted following IL-1beta and TNF-alpha treatment, whereas increased release of intracellular proteins was seen most dramatically with mechanical compression injury. Proteins involved in insulin-like growth factor and TGF-beta superfamily pathway modulation showed changes in pro-anabolic pathways that may represent early repair signals. At the systems level, two principal components were sufficient to describe 97% of the covariance in the data. A strong correlation was noted between the proteins released in response to IL-1beta and TNF-alpha; in contrast, mechanical injury resulted in both similarities and unique differences in the groups of proteins released compared with cytokine treatment.
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.