Bone Morphogenetic Protein-Mediating Receptor-Associated Smads as well as Common Smad Are Expressed in Human Articular Chondrocytes but not Up-Regulated or Down-Regulated in Osteoarthritic Cartilage

Bau, Brigitte; Haag, Jill D.; Schmid, Erik; Kaiser, Martina; Gebhard, Pia M.; Aigner, Thomas

doi:10.1359/jbmr.2002.17.12.2141

Cited by 35 publications

(30 citation statements)

References 35 publications

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“…Our previous analyses could demonstrate the expression of all three BMP-receptorassociated Smads as well as both I-Smads in adult articular chondrocytes in vivo [10,11] and supported the notion that BMP signaling is an active pathway in adult human articular cartilage.…”

Section: Introductionsupporting

confidence: 76%

“…to BMP signaling [4]. Following up this hypothesis, we were neither able to show a differential expression and/or presence of intracellular BMP-mediators (R-Smads 1, 5, 8) [11], neither of their inhibitors (I-Smads 6 and 7) [10]. However, intracellular interaction partners might alternatively significantly modulate BMP signaling (for review see Miyazono et al 2001 [20] and Hill 1999 [21]).…”

Section: Introductionmentioning

confidence: 95%

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Hgs physically interacts with Smad5 and attenuates BMP signaling

Haag

Chubinskaya

Aigner

2006

Experimental Cell Research

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Section: Introductionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 95%

Hgs physically interacts with Smad5 and attenuates BMP signaling

Haag

Chubinskaya

Aigner

2006

Experimental Cell Research

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“…The major findings reported from these studies include; a higher level of expression of both matrix metalloproteinase (MMP) 13 and ADAM-TS5 in the OA cartilage [5], up-regulation of mRNA for several collagen types in advanced OA compared to early stage OA and normal cartilage [3,18], alterations in type VI collagen distribution and appearance in OA cartilage [48], and no change in the expression level of Smads in OA versus normal cartilage [6]. Another study compared gene expression profiles between normal cartilage obtained from patients undergoing joint replacement following femoral neck fracture or obtained after foot amputation with OA cartilage obtained following knee, hip or ankle joint arthroplasty [27].…”

mentioning

confidence: 99%

Intrajoint comparisons of gene expression patterns in human osteoarthritis suggest a change in chondrocyte phenotype

Yagi

McBurney

Laverty

et al. 2005

Journal Orthopaedic Research

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Osteoarthritis (OA) is a degenerative cartilage disease with varying degrees of severity within a given joint. The purpose of this study was to define a sampling procedure for comparing human minimal and advanced OA cartilage in the same patient and to determine basic patterns of gene expression in these regions. A specific hypothesis under study was that the expression level of Bcl-2 would correlate with sox9 and aggrecan mRNA expression in vivo as has been demonstrated in vitro. Femoral condylar advanced OA cartilage was located within 1 cm of overt lesions, and minimal cartilage was taken from areas with no obvious surface defects. Histological sections were scored for disease severity and chondroitin sulfate and hydroxyproline content was determined. The expression level of nine specific genes (aggrecan, collagen type 11, Bcl-2, sox9, Link protein, osteopontin, and MMP-13, -3, and -9) was determined by quantitative real time PCR. The scores for fibrillation, chondrocyte cloning, and proteoglycan depletion were significantly different between advanced and minimal OA cartilage. The advanced OA cartilage had significantly less chondroitin sulfate than the minimal OA cartilage. Osteopontin mRNA expression showed a 3.6-fold increase in advanced compared to minimal OA cartilage. In contrast, the level of mRNA coding for aggrecan, link protein, Bcl-2, sox9 and MMP-3, -9, -13 were all decreased in advanced compared to minimal cartilage in the majority of the patients studied. Collagen type I1 mRNA expression displayed a wide-range of variation. A statistically significant correlation was observed both between Bcl-2 and sox9 mRNA level, and between Bcl-2 and aggrecan mRNA expression. The patient matched comparison of minimal and advanced OA cartilage revealed differences in cellular and tissue characteristics, and changes in gene expression that may be involved in OA progression. In addition, Bcl-2 may also play a role in regulating the expression of aggrecan through sox9 in vivo as well as in vitro.

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“…These proteins can be divided into three classes according to their functions: receptor regulated (Smads 1, 2, 3, 5, and 8), common Smad (Smad 4), and inhibitory Smads (Smads 6 and 7). Although Smads 1, 5, and 8 are specific to the BMP pathway, they do not seem to be upor down-regulated in osteoarthritic cartilage as compared with normal [2]. However, a Smad-interacting molecule, Tob1, has recently been implicated in the osteoarthritis process.…”

Section: Bone Morphogenetic Proteinsmentioning

confidence: 99%

New thoughts on the pathophysiology of osteoarthritis: One more step toward new therapeutic targets

Martel‐Pelletier

Fahmi²,

Tardif³

et al. 2006

Curr Rheumatol Rep

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Osteoarthritis is considered an illness in which a complex interaction between the tissues of the joint plays a significant role in the initiation and/or progression of this pathophysiology. We do not yet completely understand all the factors that are responsible for initiating the degradation and loss of the articular tissues. This paper summarizes the novelties of three such mechanisms. The first one points to some factors involved in the regulation of one growth factor family, the bone morphogenetic proteins, the second, the regulation of prostaglandin E(2) synthesis, and the third the factors involved in subchondral bone remodeling, all of which could be very significant events for osteoarthritis. This paper should help the reader better understand the most recent advances regarding the roles of these factors in this disease process, and how new therapeutic targets may be identified.

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Bone Morphogenetic Protein-Mediating Receptor-Associated Smads as well as Common Smad Are Expressed in Human Articular Chondrocytes but not Up-Regulated or Down-Regulated in Osteoarthritic Cartilage

Cited by 35 publications

References 35 publications

Hgs physically interacts with Smad5 and attenuates BMP signaling

Hgs physically interacts with Smad5 and attenuates BMP signaling

Intrajoint comparisons of gene expression patterns in human osteoarthritis suggest a change in chondrocyte phenotype

New thoughts on the pathophysiology of osteoarthritis: One more step toward new therapeutic targets

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