Chondrocyte phenotype and cell survival are regulated by culture conditions and by specific cytokines through the expression of Sox‐9 transcription factor

Kolettas, Evangelos; Muir, Helen; Barrett, James; Hardingham, Timothy E.

doi:10.1093/rheumatology/40.10.1146

Cited by 84 publications

(69 citation statements)

References 66 publications

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“…Similar results were observed with both ITS and Igf1, which is one of the most potent growth factors promoting cartilage maintenance and regeneration (35)(36)(37). ␤-Catenin signaling also enhances post-natal chondrocyte proliferation and is required for the maintenance of articular cartilage (20, 38 -40).…”

Section: Discussionsupporting

confidence: 59%

Histone Deacetylase 7 (Hdac7) Suppresses Chondrocyte Proliferation and β-Catenin Activity during Endochondral Ossification

Bradley

Carpio

Olson

et al. 2015

Journal of Biological Chemistry

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Background: Hdac7 is a transcriptional co-repressor in skeletal tissues, but its role in chondrocytes is undefined. Results: Proteasomal degradation reduced Hdac7 levels during chondrogenic maturation and conditional deletion of Hdac7 in chondrocytes increased proliferation and ␤-catenin levels. Conclusion: Hdac7 degradation enhances ␤-catenin transcriptional activity in growth plate chondrocytes. Significance: Suppressing Hdac7 levels increases chondrocyte proliferation and promotes cartilage formation and regeneration.

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Section: Discussionsupporting

confidence: 59%

Histone Deacetylase 7 (Hdac7) Suppresses Chondrocyte Proliferation and β-Catenin Activity during Endochondral Ossification

Bradley

Carpio

Olson

et al. 2015

Journal of Biological Chemistry

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“…Since the Cys 78 -Arg mutation in the putative IGFBP domain of WISP3 partially abolishes WISP3 function in chondrocytes, it is conceivable that WISP3 may act, in part, by augmenting the effects of IGFs. IGF-1-mediated up-regulation of cartilage ECM synthesis has already been reported by investigators at several laboratories (30)(31)(32). In addition, preliminary experimental results have demonstrated that an anti-IGF-1 neutralizing antibody partially blocks WISP3-mediated up-regulation of COL2A1 mRNA in C-28/I2 cells.…”

Section: Discussionmentioning

confidence: 54%

WISP3‐dependent regulation of type II collagen and aggrecan production in chondrocytes

Sen¹,

Cheng²,

Goldring³

et al. 2004

Arthritis & Rheumatism

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Objective. WISP3 (Wnt-1-inducible secreted protein 3) is a member of the CCN (connective tissue growth factor, cysteine-rich 61, nephroblastoma overexpressed) family of connective tissue growth factors. WISP3 mutations have been linked to progressive pseudorheumatoid dysplasia (PPRD). The present study was conducted to investigate whether WISP3 is responsible for the expression of cartilage-specific molecules.Methods. WISP3 expression in human cartilage was assessed by immunostaining with anti-WISP3 antibody. The effect of WISP3 on chondrocyte-specific gene regulation was determined by transfecting human chondrocyte lines C-28/I2 and T/C-28a2 with a WISP3 expression vector. Alterations in WISP3-mediated messenger RNA and protein expression of cartilage-specific molecules were assessed by reverse transcriptasepolymerase chain reaction and immunoblotting.Results. Immunohistochemistry experiments demonstrated that WISP3 protein is expressed in the midzone chondrocytes of normal adult articular cartilage, in chondrocyte clusters of osteoarthritic cartilage, and in the zone of proliferating chondrocytes of fetal growth cartilage. Human chondrocyte lines C-28/I2 and T/C-28a2 transfected with a WISP3 expression vector produced increased amounts of the cartilage-specific matrix molecules type II collagen and aggrecan, in part via activation of the sex-determining region Y-type high mobility group box (SOX) family of transcription factors. In contrast, a mutant WISP3, previously found to be associated with PPRD, had impaired effects on cartilage-specific gene expression.Conclusion. Our experimental results suggest that WISP3 supports cartilage integrity by regulating the expression of type II collagen and aggrecan, and mutations linked with PPRD can compromise this function and produce cartilage loss.

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“…12 The expression of sox9 in primitive mesenchymal cells induced chondrocytic phenotype: for example, the expression of cartilage-specific matrix molecules such as type II collagen and aggrecan. 19,20 In these cases, the expression of sox9 was more diffuse in the nuclei of metaplastic cells than in carcinomatous cells. S-100 protein expression in matrix-producing carcinoma, especially in metaplastic cells, is well known 2 and is frequently seen in chondrocytes and chondrocytic tumors.…”

Section: Discussionmentioning

confidence: 87%

Cartilaginous features in matrix-producing carcinoma of the breast: four cases report with histochemical and immunohistochemical analysis of matrix molecules

et al. 2008

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Matrix-producing carcinoma of the breast is a well-established entity in the group of metaplastic carcinoma, which is histologically characterized by myxochondroid matrix formation and is extremely rare. We describe here four additional cases of matrix-producing carcinoma of the breast. All cases of matrix-producing carcinoma show nest-like, sheet-like, and cord-like growth of tumor cells with cellular atypia, in addition to scattered cancer cells within myxoid or myxohyalinous stroma. Three of four cases showed an acellular or oligocellular matrix-rich zone in the center of the tumor. Immunohistochemically, cancer cells of all cases were positive for cytokeratins and epithelial membrane antigens and partially positive for sox9 and p63. Aggrecan and type II collagen, which are cartilage-specific matrix molecules, were deposited in the stroma of all cases. Type I and type IV collagens were also deposited on the stroma of all cases. These findings suggest that, although cancer cells of matrix-producing carcinoma of the breast are epithelial, they transdifferentiate to chondrocyte-like cells and produce cartilage-specific matrix molecules, which are useful markers for diagnosing matrix-producing carcinoma. Modern Pathology (2008Pathology ( ) 21, 1282Pathology ( -1292 doi:10.1038/modpathol.2008 published online 11 July 2008 Keywords: aggrecan; collagens; matrix-producing carcinoma; breast; immunohistochemistry; electron-microscopy Matrix-producing carcinoma of the breast is an extremely rare and specialized variant of metaplastic carcinoma of the breast, which is a well-established entity; 1,2 because of its rarity, the features of its stroma have remained unclear.Aggrecan is a cartilage-specific major proteoglycan. 3 This macromolecule deposits in the hypertrophic zones of growth plate cartilage, 4 although it was reported to deposit in the salivary pleomorphic adenoma, which frequently showed mesenchyme-like elements, including myxoid and chondroid tissues. 5,6 Type II collagen, which is a cartilage-specific major collagen, and chondromodulin-I (ChM-I), which is cartilage-specific noncollagenous matrix protein, 4,7,8 are deposited in the normal cartilaginous matrix. These molecules can be useful markers of cartilaginous differentiation. As sox9 is a transcription factor, the expression of which induces cartilaginous differentiation, 9-11 this molecule is also a useful marker of chondroid differentiation in normal and neoplastic tissues. [9][10][11][12] We investigated the deposition of matrix molecules in matrix-producing carcinoma of the breast, histochemically and immunohistochemically.

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Chondrocyte phenotype and cell survival are regulated by culture conditions and by specific cytokines through the expression of Sox‐9 transcription factor

Cited by 84 publications

References 66 publications

Histone Deacetylase 7 (Hdac7) Suppresses Chondrocyte Proliferation and β-Catenin Activity during Endochondral Ossification

Histone Deacetylase 7 (Hdac7) Suppresses Chondrocyte Proliferation and β-Catenin Activity during Endochondral Ossification

WISP3‐dependent regulation of type II collagen and aggrecan production in chondrocytes

Cartilaginous features in matrix-producing carcinoma of the breast: four cases report with histochemical and immunohistochemical analysis of matrix molecules

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