ArticleThe Journal of biological chemistry2010
Internalization of aggrecan G1 domain neoepitope ITEGE in chondrocytes requires CD44.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Suppression of murine osteoarthritis by 4-methylumbelliferone.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020Article
- Hyaluronan synthase 2 (HAS2) overexpression diminishes the procatabolic activity of chondrocytes by a mechanism independent of extracellular hyaluronan.The Journal of biological chemistry · 2019Article
- The pericellular hyaluronan of articular chondrocytes.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Simvastatin promotes restoration of chondrocyte morphology and phenotype.Archives of biochemistry and biophysics · 2019Article
- High molecular weight hyaluronan protects cartilage from degradation by inhibiting aggrecanase expression.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018Article
- The Zonal Architecture of the Mandibular Condyle Requires ADAMTS5.Journal of dental research · 2018Article
- CRISPR/Cas9 knockout of HAS2 in rat chondrosarcoma chondrocytes demonstrates the requirement of hyaluronan for aggrecan retention.Matrix biology : journal of the International Society for Matrix Biology · 2016Article
- 4-Methylumbelliferone Diminishes Catabolically Activated Articular Chondrocytes and Cartilage Explants via a Mechanism Independent of Hyaluronan Inhibition.The Journal of biological chemistry · 2016Article
- CD44 knock-down in bovine and human chondrocytes results in release of bound HYAL2.Matrix biology : journal of the International Society for Matrix Biology · 2015Article
- Extracellular processing of the cartilage proteoglycan aggregate and its effect on CD44-mediated internalization of hyaluronan.The Journal of biological chemistry · 2015Article
- Chondroprotective Effect of Kartogenin on CD44-Mediated Functions in Articular Cartilage and Chondrocytes.Cartilage · 2014Article
- CD44 and hyaluronan promote the bone morphogenetic protein 7 signaling response in murine chondrocytes.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Metabolism of cartilage proteoglycans in health and disease.BioMed research international · 2014Review
- Mechanisms involved in enhancement of the expression and function of aggrecanases by hyaluronan oligosaccharides.Arthritis and rheumatism · 2012Article
- Involvement of ADAMTS5 and hyaluronidase in aggrecan degradation and release from OSM-stimulated cartilage.European cells & materials · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Degradation of the cartilage proteoglycan aggrecan is one of the earliest events that occurs in association with osteoarthritis. Little is known concerning the fate of the residual N-terminal G1 domains of cleaved aggrecan; domains that remain bound to hyaluronan. In this study, 68-72-kDa bands representative of aggrecan G1 domains containing ITEGE(373) neoepitope were detected within a hyaluronidase-sensitive pool at the cell surface of bovine articular chondrocytes and within a hyaluronidase-insensitive, intracellular pool. To determine the mechanisms that contribute to this distribution, CD44 expression was knocked down by siRNA or function by CD44-DN. Both approaches prevented the retention and internalization of G1-ITEGE. Inhibition of CD44 transit into lipid rafts blocked the endocytosis of G1-ITEGE but not the retention at the cell surface. Chondrocytes derived from CD44 null mice also exhibited limited potential for retention and internalization of G1-VTEGE. The consequence of a lack of chondrocyte-mediated endocytosis of these domains in cartilage of the CD44 null mice was the accumulation of the degradation fragments within the tissue. Additionally, chondrocytes or fibroblasts derived from CD44 null mice exhibited little capacity for retention and internalization of exogenous G1-ITEGE derived from bovine cartilage explants. Bovine or wild type mouse fibroblasts were able to bind and internalize bovine-derived G1-ITEGE. Although several pathways are available for the clearance of these domains, CD44-mediated cellular internalization is the most prominent.
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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.