{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Baker N"],"funding":["NIA NIH HHS","NIAMS NIH HHS","Biotechnology and Biological Sciences Research Council"],"pagination":["2289-99"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3366172"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["64(7)"],"pubmed_abstract":["<h4>Objective</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.<h4>Methods</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"],"journal":["Arthritis and rheumatism"],"pubmed_title":["Dual regulation of metalloproteinase expression in chondrocytes by Wnt-1-inducible signaling pathway protein 3/CCN6."],"pmcid":["PMC3366172"],"funding_grant_id":["RC4 AR060546-01","RC4 AR060546","R01 AG022021-09","RC4-AR-060546","R01-AG-022021","R01 AG022021"],"pubmed_authors":["Sharpe P","Clements KM","Gavrilovic J","Baker N","Culley K","Bevan D","Otero M","Barker W","Newham P","Langham CJ","Goldring MB"],"additional_accession":[]},"is_claimable":false,"name":"Dual regulation of metalloproteinase expression in chondrocytes by Wnt-1-inducible signaling pathway protein 3/CCN6.","description":"<h4>Objective</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.<h4>Methods</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","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Jul","modification":"2025-04-03T22:33:42.535Z","creation":"2019-03-27T00:54:06Z"},"accession":"S-EPMC3366172","cross_references":{"pubmed":["22294415"],"doi":["10.1002/art.34411"]}}