Differential effects of aging on human chondrocyte responses to transforming growth factor-β: Increased pyrophosphate production and decreased cell proliferation

Rosen, Fred; McCabe, G; Quach, Jacqueline; Solan, Joell L.; Terkeltaub, Robert; Seegmiller, J. Edwin; Lotz, Martin

doi:10.1002/1529-0131(199707)40:7<1275::aid-art12>3.0.co;2-h

Cited by 36 publications

(42 citation statements)

References 31 publications

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“…Limited studies of the milk of calcium (draining lesions in JDM) document the presence of macrophages and macrophage-derived products, such as IL-6, IL-1, and TNF-α [60]. IL-1 and TNF-α [61,62] and perhaps other inflammatory mediators are regulators of extracellular pyrophosphate formation and as such may be important in the regulation of HA and calcium pyrophosphate dihydrate (CPPD) formation in soft tissues [61,62]. In JDM, calcifications occur in subcutaneous tissues including digits and elbows, and in other areas with high fat content, such as buttocks and the tail of the breast, extending to the axilla [14,63].…”

Section: Evidence That Inflammation Is a Component Of All Ha Depositimentioning

confidence: 99%

Clinical manifestations and pathogenesis of hydroxyapatite crystal deposition in juvenile dermatomyositis

Pachman

Boskey²

2006

Curr Rheumatol Rep

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Pathologic deposition of mineral in the form of bone-like hydroxyapatite is a frequent occurrence in juvenile dermatomyositis (JDM) and other connective tissue diseases. Although the sizes of the mineral crystals in JDM are similar to those in bone, there is much more mineral in the deposits than there is in bone. Bone matrix proteins also accumulate associated with the deposits. The reasons for the formation of these deposits are not known. It is our hypothesis that persistent inflammation is a component of JDM and other hydroxyapatite deposition diseases. Other contributing factors are genetic, environmental, and physical chemical. This paper discusses the influence of inflammation on the deposition of hydroxyapatite, with emphasis on the clinical and environmental factors that may facilitate the formation of calcific deposits in JDM.

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Section: Evidence That Inflammation Is a Component Of All Ha Depositimentioning

confidence: 99%

Clinical manifestations and pathogenesis of hydroxyapatite crystal deposition in juvenile dermatomyositis

Pachman

Boskey²

2006

Curr Rheumatol Rep

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“…However, since not all cells of a chondrosarcoma express p21, we suspect that the mechanism for inhibition in activity exists in the p21 pathways. Numerous studies have recently been carried out regarding the regulatory factors in chondrocyte differentiation, and growth factors -particularly TGF-β [14], IGFs [22], FGF [15], and connective tissue growth factor [19] have been reported to accelerate the proliferation and differentiation of chondrocytes. Chondrocytes or chondrosarcoma cells may be controlled by these factors in a complex manner, and studies on the interactions of these factors are needed.…”

Section: Figmentioning

confidence: 99%

“…The tumor cells of low-to intermediate-grade chondrosarcoma, which have inactive clinical behaviors and low metastatic potentials, often exhibit differentiation to chondrocytes. In chondrocytes including growth cartilage cells, many kinds of hormones, such as parathyroid hormone (PTH) [21] and parathyroid hormone related peptide (PTHrP) [1], and growth factors, such as transforming growth factor-β (TGF-β) [14], insulin-like growth factors (IGFs) [8,18,22], fibroblast growth factor (FGF) [15], and bone morphogenetic proteins (BMPs) [16] have been reported to regulate cell proliferation and differentiation.…”

Section: Introductionmentioning

confidence: 99%

Relationship of p21 (waf1/cip1) and differentiation in chondrosarcoma cells

et al. 2001

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The histological grade of chondrosarcoma correlates well with their clinical behavior and with the patient's survival duration. We have previously demonstrated that p21 was expressed in the hypertrophic chondrocytes of the growth plate. To assess the relationship of p21 (waf1/cip1) to cell differentiation in chondrosarcoma, we examined the p21 expression in 14 cases of chondrosarcoma immunohistochemically and the induction of p21 by insulin-like growth factor-I (IGF-I) during cell differentiation in SW1353 chondrosarcoma cells. p21 immunoreactivity was seen in well-differentiated chondrosarcoma cells and was mutually exclusive with MIB1 reactivity in grade-1 chondrosarcoma. In vitro, the proteoglycan synthesis of SW1353 cells was increased by IGF-I in a dose-dependent manner. However, cell proliferation was not markedly stimulated. Overexpressions of p21 mRNA and p21 protein in SW1353 cells were induced by IGF-I 100 ng/ml. Our results suggested that the p21 expression was directly related to tumor differentiation and that the p21 expression was an important mediator for IGF-I in chondrosarcoma cells.

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“…For example, experimental expression of a defective TGF␤ receptor subtype promotes terminal chondrocyte differentiation and osteoarthritis [19]. In human osteoarthritic cartilage, TGF␤ expression is significantly increased [20,21]. Moreover, in articular cartilage, hypertrophic chondrocytes surround foci of CPPD crystal deposition in chondrocalcinosis [22].…”

Section: Chondrocyte Differentiation In Mineralization: Role Of Pthrpmentioning

confidence: 99%

New developments in the pathogenesis of articular cartilage calcification

Karpouzas

Terkeltaub

1999

Curr Rheumatol Rep

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Articular cartilage, unlike growth plate cartilage, is specialized to not undergo matrix calcification. However, articular cartilage mineralization, in the form of CPPD (chondrocalcinosis) and hydroxyapatite crystals, frequently accompanies and complicates osteoarthritis and aging. Recent work has demonstrated that certain features of growth cartilage development and mineralization are shared in degenerative cartilage. These include chondrocyte proliferation, hypertrophy and increased apoptosis. Moreover, parathyroid hormone related protein (PTHrP), one of the central mediators of endochondral development, is abundant in osteoarthritic cartilage. Cartilage PPi elaboration and cytosolic transglutaminase activity are markedly increased with aging. Only recently have the molecular identities been defined for the chondrocyte inorganic pyrophosphate (PPi)-generating isozymes of the phosphodiesterase nucleotide pyrophosphatase (PDNP) family (including PC-1 and B10), and for transglutaminase in articular cartilage. This review focuses on the evolving understanding of the potential roles, in articular cartilage calcification, of PTHrP, PDNP family enzymes, PPi metabolism, and transglutaminase activity.

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Differential effects of aging on human chondrocyte responses to transforming growth factor-β: Increased pyrophosphate production and decreased cell proliferation

Abstract: These results show that aging differentially affected TGFbeta-induced PPi accumulation versus proliferation in human articular chondrocytes. These differences in TGFbeta response are likely to contribute to the development of age-associated cartilage diseases such as osteoarthritis.

Cited by 36 publications

References 31 publications

Clinical manifestations and pathogenesis of hydroxyapatite crystal deposition in juvenile dermatomyositis

Clinical manifestations and pathogenesis of hydroxyapatite crystal deposition in juvenile dermatomyositis

Relationship of p21 (waf1/cip1) and differentiation in chondrosarcoma cells

New developments in the pathogenesis of articular cartilage calcification

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