ArticleArthritis research & therapy2013
Shear stress modulates macrophage-induced urokinase plasminogen activator expression in human chondrocytes.
Article in Arthritis research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Biophysical Stimuli: A Review of Electrical and Mechanical Stimulation in Hyaline Cartilage.Cartilage · 2019Pooled it
- Low shear stress protects chondrocytes from IL-1β-induced apoptosis by activating ERK5/KLF4 signaling and negatively regulating miR-143-3p.Journal of orthopaedic surgery and research · 2024Article
- The Association of uPA, uPAR, and suPAR System with Inflammation and Joint Damage in Rheumatoid Arthritis: suPAR as a Biomarker in the Light of a Personalized Medicine Perspective.Journal of personalized medicine · 2022Article
- The role of mechanobiology in bone and cartilage model systems in characterizing initiation and progression of osteoarthritis.APL bioengineering · 2022Review
- Effects of mechanical stimulation on metabolomic profiles of SW1353 chondrocytes: shear and compression.Biology open · 2022Article
- Activation of NOTCH1 by Shear Force Elicits Immediate Cytokine Expression in Human Chondrocytes.International journal of molecular sciences · 2020Article
- Tissue Engineering and Regenerative Medicine: Achievements, Future, and Sustainability in Asia.Frontiers in bioengineering and biotechnology · 2020Review
- The antagonism of 6-shogaol in high-glucose-activated NLRP3 inflammasome and consequent calcification of human artery smooth muscle cells.Cell & bioscience · 2020Article
- Shear bioreactors stimulating chondrocyte regeneration, a systematic review.Inflammation and regeneration · 2019Review
- Fulvic acid attenuates homocysteine-induced cyclooxygenase-2 expression in human monocytes.BMC complementary and alternative medicine · 2015Article
- Construction and verification of the targeted uPA-shRNA lentiviral vector and evaluation of the transfection and silencing rate.Experimental and therapeutic medicine · 2014Article
- Serum concentrations of insulin-like growth factor-binding protein 5 in Crohn's disease.World journal of gastroenterology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSynovial macrophages, which can release proinflammatory factors, are responsible for the upregulation of cartilage-breakdown proteases and play critical roles in cartilage degradation during the progression of osteoarthritis (OA). In addition, shear stress exerts multifunctional effects on chondrocytes by inducing the synthesis of catabolic or anabolic genes. However, the interplay of macrophages, chondrocytes, and shear stress during the regulation of cartilage function remains poorly understood. We investigated the mechanisms underlying the modulation of human chondrocyte urokinase plasminogen activator (uPA) expression by macrophages and shear stress.
methodsHuman chondrocytes were stimulated by peripheral blood-macrophage- conditioned medium (PB-MCM), or exposure of chondrocytes cultured in PB-MCM to different levels of shear stress (2 to 20 dyn/cm2). Real-time polymerase chain reaction was used to analyze uPA gene expression. Inhibitors and small interfering RNA were used to investigate the mechanism for the effects of PB-MCM and shear stress in chondrocytes.
resultsStimulation of human chondrocytes with PB-MCM was found to induce uPA expression. We demonstrated that activation of the JNK and Akt pathways and NF-κB are critical for PB-MCM-induced uPA expression. Blocking assays by using IL-1ra further demonstrated that IL-1β in PB-MCM is the major mediator of uPA expression in chondrocytes. PB-MCM-treated chondrocytes subjected to a lower level of shear stress showed inhibition of MCM-induced JNK and Akt phosphorylation, NF-κB activation, and uPA expression. The PB-MCM-induced uPA expression was suppressed by AMP-activated protein kinase (AMPK) agonist. The inhibitor or siRNA for AMPK abolished the shear-mediated inhibition of uPA expression.
conclusionsThese data support the hypothesis that uPA upregulation stimulated by macrophages may play an active role in the onset of OA and in the shear-stress protection against this induction.
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