CCN family 2/connective tissue growth factor (CCN2/CTGF) stimulates proliferation and differentiation of auricular chondrocytes

Fujisawa, Takuo; Hattori, Takako; Ono, M.; Uehara, Junji; Kubota, Satoshi; Kuboki, Takuo; Takigawa, Masaharu

doi:10.1016/j.joca.2007.11.001

Cited by 50 publications

(36 citation statements)

References 16 publications

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“…Chondrocytes in adult auricular cartilage rarely express Col X. However, Col X expression could occur and inevitably trigger the terminal differentiation after a long time culture of chondrocytes, even in 3D culture [8]. In this study, supplementation of 1% ITS in 10% FBS containing medium could reduce expression of hypertrophy-related genes, such as Col X and MMP13 , indicating an inhibitory effect of ITS on hypertrophic differentiation.…”

Section: Resultsmentioning

confidence: 67%

“…In addition, dedifferentiated chondrocytes produced fewer glycosaminoglycan (GAG) and collagen type II (Col II) [6,7], which resulted in the poor cartilage tissue formation. Furthermore, undesired hypertrophy and mineralization within the engineered tissue change the features of elastic cartilage tissue [8]. These results suggested that basal chondrogenic culture medium with serum is lacks the key factors to prevent these shortages.…”

Section: Introductionmentioning

confidence: 99%

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Role of Insulin-Transferrin-Selenium in Auricular Chondrocyte Proliferation and Engineered Cartilage Formation in Vitro

Liu

Kang

et al. 2014

IJMS

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The goal of this study is to determine the effects of Insulin-Transferrin-Selenium (ITS) on proliferation of auricular chondrocytes and formation of engineered cartilage in vitro. Pig auricular monolayer chondrocytes and chondrocyte pellets were cultured in media containing 1% ITS at different concentrations of fetal bovine serum (FBS, 10%, 6%, 2%, 0%), or 10% FBS alone as a control for four weeks. Parameters including cell proliferation in monolayer, wet weight, collagen type I/II/X (Col I, II, X) and glycosaminoglycan (GAG) expression, GAG content of pellets and gene expression associated with cartilage formation/dedifferentiation (lost cartilage phenotype)/hypertrophy within the chondrocyte pellets were assessed. The results showed that chondrocytes proliferation rates increased when FBS concentrations increased (2%, 6%, 10% FBS) in ITS supplemented groups. In addition, 1% ITS plus 10% FBS significantly promoted cell proliferation than 10% FBS alone. No chondrocytes grew in ITS alone medium. 1% ITS plus 10% FBS enhanced cartilage formation in terms of size, wet weight, cartilage specific matrices, and homogeneity, compared to 10% FBS alone group. Furthermore, ITS prevented engineered cartilage from dedifferentiation (i.e., higher index of Col II/Col I mRNA expression and expression of aggrecan) and hypertrophy (i.e., lower mRNA expression of Col X and MMP13). In conclusion, our results indicated that ITS efficiently enhanced auricular chondrocytes proliferation, retained chondrogenic phenotypes, and promoted engineered cartilage formation when combined with FBS, which is potentially used as key supplementation in auricular chondrocytes and engineered cartilage culture.

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Section: Resultsmentioning

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Role of Insulin-Transferrin-Selenium in Auricular Chondrocyte Proliferation and Engineered Cartilage Formation in Vitro

Liu

Kang

et al. 2014

IJMS

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“…Although CCN2 stimulates the proliferation and differentiation of various types of chondrocytes, it does not stimulate hypertrophy of articular and auricular chondrocytes [6], [7]. CCN2 also enhances the adhesion of chondrocytes to fibronectin through integrin [8] and angiogenesis by enhancing adhesion and migration of endothelial cells in vivo [3], [9].…”

Section: Introductionmentioning

confidence: 99%

CCN Family Member 2/Connective Tissue Growth Factor (CCN2/CTGF) Has Anti-Aging Effects That Protect Articular Cartilage from Age-Related Degenerative Changes

et al. 2013

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To examine the role of connective tissue growth factor CCN2/CTGF (CCN2) in the maintenance of the articular cartilaginous phenotype, we analyzed knee joints from aging transgenic mice (TG) overexpressing CCN2 driven by the Col2a1 promoter. Knee joints from 3-, 14-, 40-, and 60-day-old and 5-, 12-, 18-, 21-, and 24-month-old littermates were analyzed. Ccn2-LacZ transgene expression in articular cartilage was followed by X-gal staining until 5 months of age. Overexpression of CCN2 protein was confirmed through all ages in TG articular cartilage and in growth plates. Radiographic analysis of knee joints showed a narrowing joint space and other features of osteoarthritis in 50% of WT, but not in any of the TG mice. Transgenic articular cartilage showed enhanced toluidine blue and safranin-O staining as well as chondrocyte proliferation but reduced staining for type X and I collagen and MMP-13 as compared with those parameters for WT cartilage. Staining for aggrecan neoepitope, a marker of aggrecan degradation in WT articular cartilage, increased at 5 and 12 months, but disappeared at 24 months due to loss of cartilage; whereas it was reduced in TG articular cartilage after 12 months. Expression of cartilage genes and MMPs under cyclic tension stress (CTS) was measured by using primary cultures of chondrocytes obtained from wild-type (WT) rib cartilage and TG or WT epiphyseal cartilage. CTS applied to primary cultures of mock-transfected rib chondrocytes from WT cartilage and WT epiphyseal cartilage induced expression of Col1a1, ColXa1, Mmp-13, and Mmp-9 mRNAs; however, their levels were not affected in CCN2-overexpressing chondrocytes and TG epiphyseal cartilage. In conclusion, cartilage-specific overexpression of CCN2 during the developmental and growth periods reduced age-related changes in articular cartilage. Thus CCN2 may play a role as an anti-aging factor by stabilizing articular cartilage.

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“…As stated in a previous section, CCN2 is also capable of enhancing the regeneration of auricular cartilage [32]. Indeed, the application of CCN2 onto the cultured auricular chondrocyte pellets enhances their growth in vivo as subcutaneous explants.…”

Section: Cartilage Regeneration By Ccn2mentioning

confidence: 70%

“…One of them is the auricular cartilage constructing the ear. Concerning the role of CCN2 in this tissue, a single report has described the effect of CCN2 on it [32]. According to this study, CCN2 promotes the proliferation and production of elastin fibers, which is one of the typical characteristics of elastic cartilage cells.…”

Section: Articular and Auricular Cartilage Formation/ Maintenancementioning

confidence: 79%

CCN2 in orofacial tissue development and remodeling

Kubota

2012

Japanese Dental Science Review

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CCN family 2/connective tissue growth factor (CCN2/CTGF) stimulates proliferation and differentiation of auricular chondrocytes

Abstract: These findings show that CCN2/CTGF may be a suitable agent for promoting differentiation and growth of auricular chondrocytes, while preventing mineralization and apoptosis, and suggests that CCN2/CTGF may be useful for the repair or reconstruction of elastic cartilage.

Cited by 50 publications

References 16 publications

Role of Insulin-Transferrin-Selenium in Auricular Chondrocyte Proliferation and Engineered Cartilage Formation in Vitro

Role of Insulin-Transferrin-Selenium in Auricular Chondrocyte Proliferation and Engineered Cartilage Formation in Vitro

CCN Family Member 2/Connective Tissue Growth Factor (CCN2/CTGF) Has Anti-Aging Effects That Protect Articular Cartilage from Age-Related Degenerative Changes

CCN2 in orofacial tissue development and remodeling

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