The Experts below are selected from a list of 156 Experts worldwide ranked by ideXlab platform
Oliver Brandau - One of the best experts on this subject based on the ideXlab platform.
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chondromodulin i is dispensable during Enchondral Ossification and eye development
Molecular and Cellular Biology, 2002Co-Authors: Oliver Brandau, Peter J Neame, Ernst B. Hunziker, Attila Aszódi, Dietmar Vestweber, Reinhard FasslerAbstract:Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor β1 (TGF-β1), TGF-β2, TGF-β3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of Enchondral Ossification.
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chondromodulin i is dispensable during Enchondral Ossification and eye development
Molecular and Cellular Biology, 2002Co-Authors: Oliver Brandau, Peter J Neame, Ernst B. Hunziker, Attila Aszódi, Dietmar Vestweber, Reinhard FasslerAbstract:Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor beta1 (TGF-beta1), TGF-beta2, TGF-beta3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of Enchondral Ossification.
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a novel gene tendin is strongly expressed in tendons and ligaments and shows high homology with chondromodulin i
Developmental Dynamics, 2001Co-Authors: Oliver Brandau, Alfons Meindl, Reinhard Fassler, Attila AszódiAbstract:Abstract Chondromodulin-I (CHM1) was identified recently as an angiogenesis inhibitor in cartilage. It is highly expressed in the avascular zones of cartilage but is absent in the late hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. Blast searches with the C-terminal part of CHM1 in available databases led to the identification of human and mouse cDNAs encoding a new protein, Tendin, that shares high homology with CHM1. Based on computer predictions, Tendin is a type II transmembrane protein containing a putative proteinase cleavage and two glycosylation sites. Northern assays with mouse RNAs demonstrated strong expression of a 1.5-kb tendin transcript in the diaphragm, skeletal muscle, and the eye and low levels of expression in all other tissues investigated. In 17.5-day-old mouse embryos, in situ hybridization revealed high levels of tendin transcript in tendons and ligaments. Additional signals were detected in brain and spinal cord, liver, lung, bowels, thymus, and eye. Cartilage, where CHM1 is found, revealed low levels of tendin m-RNA. In adult mice, tendin is expressed in neurons of all brain regions and the spinal cord. The tendin gene is localized in the human Xq22 region, to which several human diseases have been mapped. © 2001 Wiley-Liss, Inc.
Reinhard Fassler - One of the best experts on this subject based on the ideXlab platform.
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chondromodulin i is dispensable during Enchondral Ossification and eye development
Molecular and Cellular Biology, 2002Co-Authors: Oliver Brandau, Peter J Neame, Ernst B. Hunziker, Attila Aszódi, Dietmar Vestweber, Reinhard FasslerAbstract:Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor β1 (TGF-β1), TGF-β2, TGF-β3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of Enchondral Ossification.
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chondromodulin i is dispensable during Enchondral Ossification and eye development
Molecular and Cellular Biology, 2002Co-Authors: Oliver Brandau, Peter J Neame, Ernst B. Hunziker, Attila Aszódi, Dietmar Vestweber, Reinhard FasslerAbstract:Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor beta1 (TGF-beta1), TGF-beta2, TGF-beta3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of Enchondral Ossification.
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a novel gene tendin is strongly expressed in tendons and ligaments and shows high homology with chondromodulin i
Developmental Dynamics, 2001Co-Authors: Oliver Brandau, Alfons Meindl, Reinhard Fassler, Attila AszódiAbstract:Abstract Chondromodulin-I (CHM1) was identified recently as an angiogenesis inhibitor in cartilage. It is highly expressed in the avascular zones of cartilage but is absent in the late hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. Blast searches with the C-terminal part of CHM1 in available databases led to the identification of human and mouse cDNAs encoding a new protein, Tendin, that shares high homology with CHM1. Based on computer predictions, Tendin is a type II transmembrane protein containing a putative proteinase cleavage and two glycosylation sites. Northern assays with mouse RNAs demonstrated strong expression of a 1.5-kb tendin transcript in the diaphragm, skeletal muscle, and the eye and low levels of expression in all other tissues investigated. In 17.5-day-old mouse embryos, in situ hybridization revealed high levels of tendin transcript in tendons and ligaments. Additional signals were detected in brain and spinal cord, liver, lung, bowels, thymus, and eye. Cartilage, where CHM1 is found, revealed low levels of tendin m-RNA. In adult mice, tendin is expressed in neurons of all brain regions and the spinal cord. The tendin gene is localized in the human Xq22 region, to which several human diseases have been mapped. © 2001 Wiley-Liss, Inc.
N I Dolvik - One of the best experts on this subject based on the ideXlab platform.
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local morphological response of the distal femoral articular epiphyseal cartilage complex of young foals to surgical stab incision and potential relevance to cartilage injury and repair in children
Cartilage, 2013Co-Authors: Kristin Olstad, Eli H S Hendrickson, Stina Ekman, Cathy S Carlson, N I DolvikAbstract:Objective: Describe the local morphological response of the articular–epiphyseal cartilage complex to surgical stab incision in the distal femur of foals, with emphasis on the relationship between growth cartilage injury, Enchondral Ossification, and repair. Design: Nine foals were induced into general anesthesia at the age of 13 to 15 days. Four full-thickness stab incision defects were created in the cartilage on the lateral aspect of the lateral trochlear ridge of the left distal femur. Follow-up examination was carried out from 1 to 49 days postoperatively, including examination of intact bones, sawed slabs, and histological sections. Results: Incision defects filled with cells displaying fibroblast-, chondrocyte-, and osteoblast-like characteristics, potentially validating the rationale behind the drilling of stable juvenile osteochondritis dissecans lesions in children. Incisions induced necrosis within the cartilage on the margins at all depths of the defects. Sharp dissection may therefore be contraindicated in cartilage repair in young individuals. Incisions caused a focal delay in Enchondral Ossification in 2 foals, apparently related to the orientation of the incision defect relative to the direction of Ossification. Defects became progressively surrounded by subchondral bone, in which granulation tissue containing clasts and foci of osteoblast-like cells was observed. Continued Enchondral Ossification was therefore likely to result in healing of uncomplicated defects to morphologically normal bone. Conclusions: Epiphyseal growth cartilage injury had the potential to exert a negative effect on Enchondral Ossification. Enchondral Ossification exerted a beneficial effect on repair. This relationship warrants consideration in future studies of cartilage injury and repair within the articular–epiphyseal cartilage complex of all species.
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transection of vessels in epiphyseal cartilage canals leads to osteochondrosis and osteochondrosis dissecans in the femoro patellar joint of foals a potential model of juvenile osteochondritis dissecans
Osteoarthritis and Cartilage, 2013Co-Authors: Kristin Olstad, Eli H S Hendrickson, Stina Ekman, Cathy S Carlson, N I DolvikAbstract:Summary Objective To transect blood vessels within epiphyseal cartilage canals and observe whether this resulted in ischaemic chondronecrosis, an associated focal delay in Enchondral Ossification [osteochondrosis (OC)] and pathological cartilage fracture [ osteochondrosis dissecans (OCD)] in the distal femur of foals, with potential translational value to the pathogenesis of juvenile osteochondritis dissecans (JOCD) in children. Method Ten Norwegian Fjord Pony foals were operated at the age of 13–15 days. Two vessels supplying the epiphyseal growth cartilage of the lateral trochlear ridge of the left distal femur were transected in each foal. Follow-up examination was carried out from 1 to 49 days post-operatively and included plain radiography, macroscopic and histological examination. Results Transection of blood vessels within epiphyseal cartilage canals resulted in necrosis of vessels and chondrocytes, i.e., ischaemic chondronecrosis, in foals. Areas of ischaemic chondronecrosis were associated with a focal delay in Enchondral Ossification (OC) in foals examined 21 days or more after transection, and pathological cartilage fracture (OCD) in one foal examined 42 days after transection. Conclusion The ischaemic hypothesis for the pathogenesis of OC has been reproduced experimentally in foals. There are several similarities between OCD in animals and JOCD in children. It should be investigated whether JOCD also occurs due to a focal failure in the cartilage canal blood supply, followed by ischaemic chondronecrosis.
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early lesions of osteochondrosis in the distal tibia of foals
Journal of Orthopaedic Research, 2007Co-Authors: Kristin Olstad, Stina Ekman, Cathy S Carlson, Bjornar Ytrehus, N I DolvikAbstract:Material available for research into osteochondrosis (OC) in humans tends to represent chronic lesions. Comparative studies of early lesions in young animals are, therefore, important in clarifying the pathogenesis of OC in humans. Recent studies in pigs provide strong evidence that lesions of articular OC are associated with a focal failure in the cartilage canal vascular supply to epiphyseal growth cartilage (articular–epiphyseal cartilage complex excluding the articular cartilage). The purpose of the present study was to examine histological sections from a specific predilection site for articular OC in the distal tibia of a large number of young foals to determine if the same is true in horses. Material from the distal tibiae of 100 foals aged from 191 days of gestation to 153 days old was collected from routine submissions of fetuses and foals for post mortem examination. The tibiae were band-sawed into slabs, and selected slabs were processed for histology, stained with hematoxylin and eosin, and examined using light microscopy. Early subclinical developmental stages of OC were found in the most common site for clinical OC lesions of horses in nine of 100 foals aged 12 to 122 days old. All lesions contained areas of chondrocyte necrosis that were associated with cartilage canal necrosis in five of nine foals. Five of these foals also had focal disruption of Enchondral Ossification at the chondro–osseous junction in the same site. Early lesions purported to play a role in the initial stages of articular OC in the distal tibia of horses were characterized by chondrocyte necrosis and likely occurred secondary to a failure of cartilage canal vascular supply to epiphyseal growth cartilage. The similarities in appearance between early lesions of piglets and foals suggest that information gained in one species may be transferable to others, including humans. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:1094–1105, 2007
Attila Aszódi - One of the best experts on this subject based on the ideXlab platform.
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chondromodulin i is dispensable during Enchondral Ossification and eye development
Molecular and Cellular Biology, 2002Co-Authors: Oliver Brandau, Peter J Neame, Ernst B. Hunziker, Attila Aszódi, Dietmar Vestweber, Reinhard FasslerAbstract:Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor β1 (TGF-β1), TGF-β2, TGF-β3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of Enchondral Ossification.
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chondromodulin i is dispensable during Enchondral Ossification and eye development
Molecular and Cellular Biology, 2002Co-Authors: Oliver Brandau, Peter J Neame, Ernst B. Hunziker, Attila Aszódi, Dietmar Vestweber, Reinhard FasslerAbstract:Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor beta1 (TGF-beta1), TGF-beta2, TGF-beta3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of Enchondral Ossification.
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a novel gene tendin is strongly expressed in tendons and ligaments and shows high homology with chondromodulin i
Developmental Dynamics, 2001Co-Authors: Oliver Brandau, Alfons Meindl, Reinhard Fassler, Attila AszódiAbstract:Abstract Chondromodulin-I (CHM1) was identified recently as an angiogenesis inhibitor in cartilage. It is highly expressed in the avascular zones of cartilage but is absent in the late hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. Blast searches with the C-terminal part of CHM1 in available databases led to the identification of human and mouse cDNAs encoding a new protein, Tendin, that shares high homology with CHM1. Based on computer predictions, Tendin is a type II transmembrane protein containing a putative proteinase cleavage and two glycosylation sites. Northern assays with mouse RNAs demonstrated strong expression of a 1.5-kb tendin transcript in the diaphragm, skeletal muscle, and the eye and low levels of expression in all other tissues investigated. In 17.5-day-old mouse embryos, in situ hybridization revealed high levels of tendin transcript in tendons and ligaments. Additional signals were detected in brain and spinal cord, liver, lung, bowels, thymus, and eye. Cartilage, where CHM1 is found, revealed low levels of tendin m-RNA. In adult mice, tendin is expressed in neurons of all brain regions and the spinal cord. The tendin gene is localized in the human Xq22 region, to which several human diseases have been mapped. © 2001 Wiley-Liss, Inc.
Dietmar Vestweber - One of the best experts on this subject based on the ideXlab platform.
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chondromodulin i is dispensable during Enchondral Ossification and eye development
Molecular and Cellular Biology, 2002Co-Authors: Oliver Brandau, Peter J Neame, Ernst B. Hunziker, Attila Aszódi, Dietmar Vestweber, Reinhard FasslerAbstract:Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor β1 (TGF-β1), TGF-β2, TGF-β3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of Enchondral Ossification.
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chondromodulin i is dispensable during Enchondral Ossification and eye development
Molecular and Cellular Biology, 2002Co-Authors: Oliver Brandau, Peter J Neame, Ernst B. Hunziker, Attila Aszódi, Dietmar Vestweber, Reinhard FasslerAbstract:Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during Enchondral Ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor beta1 (TGF-beta1), TGF-beta2, TGF-beta3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of Enchondral Ossification.