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- Publisher Website: 10.1007/s00296-008-0744-z
- Scopus: eid_2-s2.0-61449135868
- PMID: 18941754
- WOS: WOS:000263781500007
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Article: Expression of ADAMTS-4 by chondrocytes in the surface zone of human osteoarthritic cartilage is regulated by epigenetic DNA de-methylation
Title | Expression of ADAMTS-4 by chondrocytes in the surface zone of human osteoarthritic cartilage is regulated by epigenetic DNA de-methylation |
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Authors | |
Keywords | ADAMTS-4 |
Issue Date | 2009 |
Citation | Rheumatology International, 2009, v. 29, n. 5, p. 525-534 How to Cite? |
Abstract | The two major aggrecanases involved in osteoarthritis (OA) are ADAMTS-4 and ADAMTS-5. Knock-out studies suggested that ADAMTS-5, but not ADAMTS-4, is the major aggrecanase in murine OA. However, studies of human articular cartilage suggest that ADAMTS-4 also contributes to aggrecan degradation in human OA. This study investigated ADAMTS-4 in human OA. While ADAMTS-4 was virtually absent in control cartilage, numerous ADAMTS-4 immuno-positive chondrocytes were present in OA cartilage and their numbers increased with disease severity. RT-PCR confirmed expression, especially in the surface zone. DNA methylation was lost at specific CpG sites in the ADAMTS-4 promoter in OA chondrocytes, suggesting that the increased gene expression was more than a simple up-regulation, but involved loss of DNA methylation at specific CpG sites, resulting in a heritable and permanent expression of ADAMTS-4 in OA chondrocytes. These results suggest that ADAMTS-4 is epigenetically regulated and plays a role in aggrecan degradation in human OA. © 2008 Springer-Verlag. |
Persistent Identifier | http://hdl.handle.net/10722/228069 |
ISSN | 2023 Impact Factor: 3.2 2023 SCImago Journal Rankings: 0.971 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Cheung, Kelvin S C | - |
dc.contributor.author | Hashimoto, Ko | - |
dc.contributor.author | Yamada, Norikazu | - |
dc.contributor.author | Roach, Helmtrud I. | - |
dc.date.accessioned | 2016-08-01T06:45:06Z | - |
dc.date.available | 2016-08-01T06:45:06Z | - |
dc.date.issued | 2009 | - |
dc.identifier.citation | Rheumatology International, 2009, v. 29, n. 5, p. 525-534 | - |
dc.identifier.issn | 0172-8172 | - |
dc.identifier.uri | http://hdl.handle.net/10722/228069 | - |
dc.description.abstract | The two major aggrecanases involved in osteoarthritis (OA) are ADAMTS-4 and ADAMTS-5. Knock-out studies suggested that ADAMTS-5, but not ADAMTS-4, is the major aggrecanase in murine OA. However, studies of human articular cartilage suggest that ADAMTS-4 also contributes to aggrecan degradation in human OA. This study investigated ADAMTS-4 in human OA. While ADAMTS-4 was virtually absent in control cartilage, numerous ADAMTS-4 immuno-positive chondrocytes were present in OA cartilage and their numbers increased with disease severity. RT-PCR confirmed expression, especially in the surface zone. DNA methylation was lost at specific CpG sites in the ADAMTS-4 promoter in OA chondrocytes, suggesting that the increased gene expression was more than a simple up-regulation, but involved loss of DNA methylation at specific CpG sites, resulting in a heritable and permanent expression of ADAMTS-4 in OA chondrocytes. These results suggest that ADAMTS-4 is epigenetically regulated and plays a role in aggrecan degradation in human OA. © 2008 Springer-Verlag. | - |
dc.language | eng | - |
dc.relation.ispartof | Rheumatology International | - |
dc.subject | ADAMTS-4 | - |
dc.title | Expression of ADAMTS-4 by chondrocytes in the surface zone of human osteoarthritic cartilage is regulated by epigenetic DNA de-methylation | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1007/s00296-008-0744-z | - |
dc.identifier.pmid | 18941754 | - |
dc.identifier.scopus | eid_2-s2.0-61449135868 | - |
dc.identifier.volume | 29 | - |
dc.identifier.issue | 5 | - |
dc.identifier.spage | 525 | - |
dc.identifier.epage | 534 | - |
dc.identifier.isi | WOS:000263781500007 | - |
dc.identifier.f1000 | 725822264 | - |
dc.identifier.issnl | 0172-8172 | - |