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Data from three wild-type and two <jats:italic>Frzb<\/jats:italic><jats:sup>\n                              <jats:italic>-\/-<\/jats:italic>\n                           <\/jats:sup> samples could be used for pathway analysis of differentially expressed genes and were explored with PANTHER, DAVID and GSEA bioinformatics tools. Activation of the wingless-type (WNT) pathway was analysed using Western blot. The effects of <jats:italic>Frzb<\/jats:italic> gain and loss of function on chondrogenesis and cell proliferation was examined using ATDC5 micro-masses and mouse ribcage chondrocytes.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Results<\/jats:title>\n                        <jats:p>Extracellular matrix-associated integrin and cadherin pathways, as well as WNT pathway genes were up-regulated in <jats:italic>Frzb<\/jats:italic><jats:sup>\n                              <jats:italic>-\/-<\/jats:italic>\n                           <\/jats:sup> samples. Several WNT receptors, target genes and other antagonists were up-regulated, but no difference in active \u03b2-catenin was found. Analysis of ATDC5 cell micro-masses overexpressing <jats:italic>FRZB<\/jats:italic> indicated an up-regulation of <jats:italic>aggrecan<\/jats:italic> and <jats:italic>Col2a1<\/jats:italic>, and down-regulation of molecules related to damage and repair in cartilage, <jats:italic>Col3a1<\/jats:italic> and <jats:italic>Col5a1<\/jats:italic>. Silencing of <jats:italic>Frzb<\/jats:italic> resulted in down-regulation of <jats:italic>aggrecan<\/jats:italic> and <jats:italic>Col2a1<\/jats:italic>. Pathways associated with cell cycle were down-regulated in this transcriptome analysis. Ribcage chondrocytes derived from <jats:italic>Frzb<\/jats:italic><jats:sup>\n                              <jats:italic>-\/-<\/jats:italic>\n                           <\/jats:sup> mice showed decreased proliferation compared to wild-type cells.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Conclusions<\/jats:title>\n                        <jats:p>Our analysis provides evidence for tight regulation of WNT signalling, shifts in extracellular matrix components and effects on cell proliferation and differentiation in the articular cartilage - subchondral bone unit in <jats:italic>Frzb<\/jats:italic><jats:sup>\n                              <jats:italic>-\/-<\/jats:italic>\n                           <\/jats:sup> mice. These data further support an important role for FRZB in joint homeostasis and highlight the complex biology of WNT signaling in the joint.<\/jats:p>\n                     <\/jats:sec>","DOI":"10.1186\/ar3695","type":"journal-article","created":{"date-parts":[[2012,1,20]],"date-time":"2012-01-20T19:40:55Z","timestamp":1327088455000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Tight regulation of wingless-type signaling in the articular cartilage - subchondral bone biomechanical unit: transcriptomics in Frzb-knockout mice"],"prefix":"10.1186","volume":"14","author":[{"given":"Liesbet","family":"Lodewyckx","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fr\u00e9d\u00e9ric","family":"Cailotto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Thysen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank P","family":"Luyten","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rik J","family":"Lories","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2012,1,20]]},"reference":[{"key":"3541_CR1","doi-asserted-by":"publisher","first-page":"209","DOI":"10.1016\/j.berh.2007.12.001","volume":"22","author":"RJ Lories","year":"2008","unstructured":"Lories RJ: Joint homeostasis, restoration, and remodeling in osteoarthritis. 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