ArticleThe Journal of biological chemistry2015
Autophagy modulates articular cartilage vesicle formation in primary articular chondrocytes.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- From pathogenesis to therapy: extracellular vesicles in osteoarthritis.Frontiers in bioengineering and biotechnology · 2026Review
- Systematic druggable genome-wide Mendelian randomization identifies therapeutic targets for calcium pyrophosphate deposition disease.Clinical rheumatology · 2025Article
- Extracellular Vesicles: A Novel Diagnostic Tool and Potential Therapeutic Approach for Equine Osteoarthritis.Current issues in molecular biology · 2024Review
- Bone marrow stromal and anterior cruciate ligament remnant cell co-culture-derived extracellular vesicles promote cell activity in both cell types.Journal of cellular and molecular medicine · 2024Article
- β1-Integrin-Mediated Uptake of Chondrocyte Extracellular Vesicles Regulates Chondrocyte Homeostasis.International journal of molecular sciences · 2024Article
- Exosomal communication: a pivotal regulator of bone homeostasis and a potential therapeutic target.Frontiers in pharmacology · 2024Review
- Chondrocyte Homeostasis and Differentiation: Transcriptional Control and Signaling in Healthy and Osteoarthritic Conditions.Life (Basel, Switzerland) · 2023Review
- Exosomes: Diagnostic and Therapeutic Implications in Cancer.Pharmaceutics · 2023Review
- Article
- Insights into Exosome in the Intervertebral Disc: Emerging Role for Disc Homeostasis and Normal Function.International journal of medical sciences · 2022Review
- Chondrogenic differentiation induced by extracellular vesicles bound to a nanofibrous substrate.NPJ Regenerative medicine · 2021Article
- Exosomes Immunity Strategy: A Novel Approach for Ameliorating Intervertebral Disc Degeneration.Frontiers in cell and developmental biology · 2021Review
- Articular chondrocyte-derived extracellular vesicles promote cartilage differentiation of human umbilical cord mesenchymal stem cells by activation of autophagy.Journal of nanobiotechnology · 2020Article
- Non-viral Gene Delivery Methods for Bone and Joints.Frontiers in bioengineering and biotechnology · 2020Review
- Mutations in osteoprotegerin account for the CCAL1 locus in calcium pyrophosphate deposition disease.Osteoarthritis and cartilage · 2018Article
- Matrix vesicles from chondrocytes and osteoblasts: Their biogenesis, properties, functions and biomimetic models.Biochimica et biophysica acta. General subjects · 2018Review
- Role of the Inflammation-Autophagy-Senescence Integrative Network in Osteoarthritis.Frontiers in physiology · 2018Review
- Extracellular vesicles in cartilage homeostasis and osteoarthritis.Current opinion in rheumatology · 2018Review
- Lipid Tales of Viral Replication and Transmission.Trends in cell biology · 2017Review
- The Autophagic Machinery in Viral Exocytosis.Frontiers in microbiology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Chondrocyte-derived extracellular organelles known as articular cartilage vesicles (ACVs) participate in non-classical protein secretion, intercellular communication, and pathologic calcification. Factors affecting ACV formation and release remain poorly characterized; although in some cell types, the generation of extracellular vesicles is associated with up-regulation of autophagy. We sought to determine the role of autophagy in ACV production by primary articular chondrocytes. Using an innovative dynamic model with a light scatter nanoparticle counting apparatus, we determined the effects of autophagy modulators on ACV number and content in conditioned medium from normal adult porcine and human osteoarthritic chondrocytes. Healthy articular chondrocytes release ACVs into conditioned medium and show significant levels of ongoing autophagy. Rapamycin, which promotes autophagy, increased ACV numbers in a dose- and time-dependent manner associated with increased levels of autophagy markers and autophagosome formation. These effects were suppressed by pharmacologic autophagy inhibitors and short interfering RNA for ATG5. Caspase-3 inhibition and a Rho/ROCK inhibitor prevented rapamycin-induced increases in ACV number. Osteoarthritic chondrocytes, which are deficient in autophagy, did not increase ACV number in response to rapamycin. SMER28, which induces autophagy via an mTOR-independent mechanism, also increased ACV number. ACVs induced under all conditions had similar ecto-enzyme specific activities and types of RNA, and all ACVs contained LC3, an autophagosome-resident protein. These findings identify autophagy as a critical participant in ACV formation, and augment our understanding of ACVs in cartilage disease and repair.
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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.