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• W2800300596 abstract "Purpose: CEMIP for “Cell migration-inducing and hyaluronan-binding protein”expression is increased in various cancers and described as a key regulator of cell mortality, growth and invasion. In rheumatoid arthritis CEMIP is referred to as an angiogenic marker and participates in hyaluronic acid degradation. In the present study, the expression of CEMIP is investigated in healthy and OA cartilage. Its role in the physiopathology of OA is unraveled, specifically in cell proliferation, in chondrocyte dedifferentiation and in the extracellular matrix remodeling but also in newly acquired functions in fibrosis. Methods: CEMIP expression was assessed by immunohistochemistry on cartilage obtained from patients with osteoarthritis undergoing knee (or hip) replacement surgery or having a subcapital femoral fracture (non-osteoarthritic cartilage). CEMIP expression was also investigated by immunohistochemistry in the cartilage of mice for which osteoarthritis was induced either by destabilization of the internal meniscus or by intra-articular injection of collagenase. The expression of CEMIP was studied in vitro using a dedifferentiated model comparing human freshly isolated knee OA chondrocytes cultivated in monolayer culture during 1, 4 or 14 days. The high-throughput sequencing of the entire transcriptome was performed on the total RNA of human OA knee dedifferentiated chondrocytes expressing or not CEMIP. CEMIP expression was silenced using two different specific lentiviral shRNA. An anti-EGFP shRNA was used as control. A Gene Set Enrichment Analysis (GSEA) was conducted to highlight the different signaling pathways impacted by the absence of CEMIP. The level of expression of different genes was assessed by RT-qPCR. The expression level of the proteins was analyzed by western blot or ELISA. Results: CEMIP is overexpressed in human and mouse OA cartilage compared to healthy cartilage. In vitro, the CEMIP level of isolated human chondrocytes is increased in dedifferentiated chondrocytes after 14 days of monolayer culture compared to freshly isolated chondrocytes. GSEA highlighted 2675 genes that were significantly down or up-regulated in CEMIP depleted cells (with both shRNA) compared to control cells (p<0.001). Among them, 56 had a shrunk Log2 fold change higher than +/-1 and several genes were involved in cartilage turnover, mesenchymal transition and fibrosis. Indeed, increased expression levels of types I, III, IV and V collagen mRNA and less type II, VI, IX and XI were observed in dedifferentiated chondrocytes expressing CEMIP compared to chondrocytes for which CEMIP expression was abrogated. CEMIP depletion also induced a modulation of genes belonging to the mesenchymal transition pathway (GSEA) with, among others, a decreased periostin secretion (and POSTN mRNA) and β-catenin protein level (but not mRNA). CEMIP also promoted αSMA expression and TGF-β signaling towards the p-Smad2-3/Alk5/PAI-1 pathway. Additionally, we demonstrated that CEMIP is essential for chondrocytes proliferation triggered by TGF-β. This sustains the hypothesis that CEMIP is a cell proliferator inducer. Conclusions: CEMIP was increased in OA and participated to human chondrocyte dedifferentiation into a fibroblast-like chondrocyte and its transdifferentiation into an activated myofibroblast expressing αSMA. CEMIP induced a fibrotic response through the Wnt/β-Catenin and the TGF-β pathway." @default.
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• W2800300596 date "2018-04-01" @default.
• W2800300596 modified "2023-09-28" @default.
• W2800300596 title "Cemip is a new key regulator of chondrocytes transdifferentiation involved in osteoarthritic cartilage fibrosis" @default.
• W2800300596 doi "https://doi.org/10.1016/j.joca.2018.02.204" @default.
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