<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Baker N</submitter><funding>NIA NIH HHS</funding><funding>NIAMS NIH HHS</funding><funding>Biotechnology and Biological Sciences Research Council</funding><pagination>2289-99</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3366172</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>64(7)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>Wnt-1-inducible signaling pathway protein 3 (WISP-3)/CCN6 is mutated in progressive pseudorheumatoid dysplasia and may have effects on cartilage homeostasis. The aim of this study was to ascertain additional roles for WISP-3/CCN6 by determining its expression in osteoarthritic (OA) cartilage and by investigating its effects on cartilage-relevant metalloproteinase expression in immortalized (C-28/I2) and primary chondrocytes.&lt;h4>Methods&lt;/h4>Cartilage steady-state levels of WISP-3/CCN6 messenger RNA and protein production were determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry, respectively. WISP-3/CCN6 was overexpressed in C-28/I2 cells, and the resultant clones were analyzed by quantitative RT-PCR. The st</pubmed_abstract><journal>Arthritis and rheumatism</journal><pubmed_title>Dual regulation of metalloproteinase expression in chondrocytes by Wnt-1-inducible signaling pathway protein 3/CCN6.</pubmed_title><pmcid>PMC3366172</pmcid><funding_grant_id>RC4 AR060546-01</funding_grant_id><funding_grant_id>RC4 AR060546</funding_grant_id><funding_grant_id>R01 AG022021-09</funding_grant_id><funding_grant_id>RC4-AR-060546</funding_grant_id><funding_grant_id>R01-AG-022021</funding_grant_id><funding_grant_id>R01 AG022021</funding_grant_id><pubmed_authors>Sharpe P</pubmed_authors><pubmed_authors>Clements KM</pubmed_authors><pubmed_authors>Gavrilovic J</pubmed_authors><pubmed_authors>Baker N</pubmed_authors><pubmed_authors>Culley K</pubmed_authors><pubmed_authors>Bevan D</pubmed_authors><pubmed_authors>Otero M</pubmed_authors><pubmed_authors>Barker W</pubmed_authors><pubmed_authors>Newham P</pubmed_authors><pubmed_authors>Langham CJ</pubmed_authors><pubmed_authors>Goldring MB</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dual regulation of metalloproteinase expression in chondrocytes by Wnt-1-inducible signaling pathway protein 3/CCN6.</name><description>&lt;h4>Objective&lt;/h4>Wnt-1-inducible signaling pathway protein 3 (WISP-3)/CCN6 is mutated in progressive pseudorheumatoid dysplasia and may have effects on cartilage homeostasis. The aim of this study was to ascertain additional roles for WISP-3/CCN6 by determining its expression in osteoarthritic (OA) cartilage and by investigating its effects on cartilage-relevant metalloproteinase expression in immortalized (C-28/I2) and primary chondrocytes.&lt;h4>Methods&lt;/h4>Cartilage steady-state levels of WISP-3/CCN6 messenger RNA and protein production were determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry, respectively. WISP-3/CCN6 was overexpressed in C-28/I2 cells, and the resultant clones were analyzed by quantitative RT-PCR. The st</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Jul</publication><modification>2025-04-03T22:33:42.535Z</modification><creation>2019-03-27T00:54:06Z</creation></dates><accession>S-EPMC3366172</accession><cross_references><pubmed>22294415</pubmed><doi>10.1002/art.34411</doi></cross_references></HashMap>