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Dive into the research topics where Brigitte Bau is active.

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Featured researches published by Brigitte Bau.


Matrix Biology | 2003

SOX9 expression does not correlate with type II collagen expression in adult articular chondrocytes.

Thomas Aigner; Pia M. Gebhard; Erik Schmid; Brigitte Bau; Vincent R. Harley; Ernst Pöschl

Anabolic activity is a crucial activity of articular chondrocytes and its failure is one major reason of osteoarthritic cartilage degeneration. The intracellular factors responsible for the increase or decrease of anabolic activity of articular chondrocytes remain largely unknown. A recent candidate, the transcription factor SOX9, has elicited much interest as it is suggested to be a central factor in chondrocytic differentiation during development, including collagen type II (COL2A1) expression, the major anabolic gene product of chondrocytes. Here we show that normal adult human articular chondrocytes in vivo contain high SOX9 mRNA levels, which are decreased in osteoarthritic cartilage. Surprisingly, no positive correlation between SOX9 and COL2A1 expression was observed--to the contrary, the expression of COL2A1 was significantly increased in the diseased cells. Immunolocalization confirmed the presence of SOX9 protein in normal and osteoarthritic chondrocytes without showing significant differences in both SOX9 quantity and subcellular localization in osteoarthritic compared to normal cartilage tissue. Interestingly, laser scanning confocal microscopy showed that the subcellular distribution of SOX9 in adult chondrocytes was not restricted to the nucleus as observed in fetal chondrocytes, but was also detected within the cytoplasm, with no differences in subcellular SOX9 distribution between normal and OA cartilage. This is consistent with the lack of positive correlation between SOX9 and COL2A1 expression in adult articular chondrocytes. Also, no positive correlation between SOX9 and COL2A1 expression was observed in vitro after challenge of chondrocytes with Il-1beta, which is a strong (negative) regulator of COL2A1 expression, or with IGF-I, which stimulates COL2A1 expression. These results suggest that SOX9 is not the key regulator of COL2A1 promoter activity in human adult articular chondrocytes. However, SOX9 might still be involved in maintaining the chondrocytic phenotype in normal and osteoarthritic cartilage.


Journal of Orthopaedic Research | 2003

Quantification of expression levels of cellular differentiation markers does not support a general shift in the cellular phenotype of osteoarthritic chondrocytes

Pia M. Gebhard; Angelika Gehrsitz; Brigitte Bau; Stephan Söder; Wolfgang Eger; Thomas Aigner

Many studies have shown increased anabolic activity in osteoarthritic cartilage and have suggested changes in the cellular phenotypes of articular chondrocytes. Most of these studies relied on non‐quantitative technologies, which did not allow the estimation of the relative importance of the different differentiation phenomena. In the present study, we developed and used quantitative PCR assays for collagen types I, II(total), IIA, III, and X as marker genes indicating cellular synthetic activity (collagen type II) as well as differentiation pattern of chondrocytes (collagen types I, IIA, III, and X) and quantified these genes in normal, early degenerative, and late stage osteoarthritic cartilage in parallel.


Rheumatology International | 2006

Role of mitogen-activated protein kinases and NFκB on IL-1β-induced effects on collagen type II, MMP-1 and 13 mRNA expression in normal articular human chondrocytes

Zhiyong Fan; Huiqing Yang; Brigitte Bau; Stephan Söder; Thomas Aigner

Interleukin-1ß is a pro-inflammatory cytokine that causes anti-anabolic and catabolic effects on articular chondrocytes via four major signaling pathways. In this study, we investigated the role of these pathways for the repression of collagen type II, and induction of MMP-1 and -13 by Il-1ß. Human adult chondrocytes were stimulated with IL-1β together with selective inhibitors of the ERK, JNK, p38, and NFκB pathways. Inhibitors of ERK and NFκB could significantly block the induction of MMP-1 and -13 (p<0.05) and the repression of collagen type II (p<0.01). The inhibitor for p38 MAPK was able to block partially MMP-1 and -13 up-regulation (p<0.01), but did not significantly inhibit collagen type II repression. Our data suggest that ERK and NFkB pathways are particularly important for IL-1β regulating collagen type II and MMP-1 and -13 expression and that p38, but not JNK is additionally involved in MMP-1 and -13 induction.


Journal of Bone and Mineral Research | 2002

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

Brigitte Bau; Jochen Haag; Erik Schmid; Martina Kaiser; Pia M. Gebhard; Thomas Aigner

Bone morphogenetic proteins (BMPs) are supposed to be important for cartilage matrix anabolism. In this study, we investigated whether the intracellular mediators of BMP activity, Smads 1, 4, 5, and 8, are expressed in normal human articular chondrocytes in vivo and in vitro and whether alterations in expression and distribution pattern are found in osteoarthritic cartilage or in vitro after stimulation with interleukin (IL)‐1, because down‐regulation of these mediators could be responsible for the decrease of anabolic activity in osteoarthritic cartilage. RNA was isolated from normal and osteoarthritic human knee cartilage and analyzed by (quantitative) polymerase chain reaction (PCR) technology. Articular chondrocytes were cultured in alginate beads and short‐term high‐density monolayer cultures with and without stimulation by IL‐1. In addition, immunolocalization of the receptor‐associated Smads (R‐Smads) was performed on sections of normal and diseased articular cartilage. Reverse‐transcription (RT)‐PCR analysis showed a moderate expression of all Smads investigated in normal, early degenerative, and late stage osteoarthritic cartilage. Immunolocalization detected the R‐Smads in most chondrocytes on the protein level in all specimen groups investigated. In vitro, the Smads were also expressed and partly up‐regulated by Il‐1β in alginate bead culture. Of note, for Smad 1, two truncated splice variants were expressed by articular chondrocytes missing exon 4 as well as exons 3 and 4. Our study showed that BMP‐receptor Smads 1, 5, and 8 as well as common Smad (C‐Smad) 4 are expressed and present in human normal and osteoarthritic articular chondrocytes corroborating the importance of BMPs and BMP signaling for articular cartilage. This study is the first to describe splicing variants for Smad 1. Smads 1, 4, and 5 are up‐regulated in vitro by Il‐1β, suggesting a linkage of the Il‐1 and BMP‐signaling pathways within the chondrocytes. None of the Smads were grossly up‐ or down‐regulated in osteoarthritic chondrocytes, suggesting that differences in overall expression levels of the investigated Smad proteins are not relevant for metabolic activity of articular chondrocytes in vivo.


Methods in molecular medicine | 2004

Quantification of mRNA Expression Levels in Articular Chondrocytes With PCR Technologies

Audrey McAlinden; Jochen Haag; Brigitte Bau; Pia M. Gebhard; Thomas Aigner

Unlike any other technology in molecular biology, the polymerase chain reaction (PCR) has changed the technological armamentarium of molecular scientists working on cartilage, in terms of outstanding sensitivity and accuracy. Four approaches to determine mRNA expression levels by PCR amplification of specific cDNA sequences are currently in use and are discussed in this chapter: conventional PCR with end-point determination, conventional PCR in the logarithmic amplification phase, conventional PCR using internal competitive DNA fragments, and real-time PCR as offered by TaqMan technology and others. The determination of mRNA expression levels by real-time quantitative PCR appears to be the most reliable method for accurate determination of gene expression levels within cartilage and cultured chondrocytes, as in other tissues and cell types. This technology offers outstanding sensitivity and accuracy in terms of determination of the amount of cDNA molecules. However, this method cannot account for factors such as efficiency of RNA isolation and reverse transcription conditions. Thus, normalization of the acquired data is required, with all its limitations as described.


Arthritis & Rheumatism | 2002

Relative messenger RNA expression profiling of collagenases and aggrecanases in human articular chondrocytes in vivo and in vitro

Brigitte Bau; Pia M. Gebhard; Jochen Haag; Thomas Knorr; Eckart Bartnik; Thomas Aigner


Arthritis & Rheumatism | 2005

Freshly isolated osteoarthritic chondrocytes are catabolically more active than normal chondrocytes, but less responsive to catabolic stimulation with interleukin-1

Zhiyong Fan; Brigitte Bau; Huiqing Yang; Stephan Soeder; Thomas Aigner


Cytokine | 2004

IL-1β induction of IL-6 and LIF in normal articular human chondrocytes involves the ERK, p38 and NFκB signaling pathways

Zhiyong Fan; Brigitte Bau; Huiqing Yang; Thomas Aigner


Arthritis & Rheumatism | 2004

Bone morphogenetic protein and transforming growth factor β inhibitory Smads 6 and 7 are expressed in human adult normal and osteoarthritic cartilage in vivo and are differentially regulated in vitro by interleukin‐1β

Martina Kaiser; Jochen Haag; Stephan Söder; Brigitte Bau; Thomas Aigner


The Journal of Rheumatology | 2004

ADAMTS-1, a gene product of articular chondrocytes in vivo and in vitro, is downregulated by interleukin 1beta.

Lydia Wachsmuth; Brigitte Bau; Zhiyong Fan; Anja Pecht; Nicole Gerwin; Thomas Aigner

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Pia M. Gebhard

University of Erlangen-Nuremberg

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Zhiyong Fan

University of Erlangen-Nuremberg

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Jochen Haag

University of Erlangen-Nuremberg

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Huiqing Yang

University of Erlangen-Nuremberg

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Stephan Söder

University of Erlangen-Nuremberg

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Anja Pecht

University of Erlangen-Nuremberg

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Erik Schmid

University of Erlangen-Nuremberg

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Martina Kaiser

University of Erlangen-Nuremberg

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Stephan Soeder

University of Erlangen-Nuremberg

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