The Experts below are selected from a list of 12336 Experts worldwide ranked by ideXlab platform
Bing Zhang - One of the best experts on this subject based on the ideXlab platform.
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different roles of akt and mechanistic target of rapamycin in serum dependent chondroprotection of human osteoarthritic Chondrocytes
International Journal of Molecular Medicine, 2017Co-Authors: Tongen Zhang, Xinpeng Zheng, Bing ZhangAbstract:: Despite various animal serums being used widely to Culture Chondrocytes, the regulatory mechanism of serum on chondrocyte activities has not been elucidated. In the present study, human osteoarthritis (OA) Chondrocytes were used to perform in vitro investigations on the effect of different concentrations of bovine fetal serum on extracellular matrix synthesis, cell proliferation and autophagy using the Cell Counting Kit‑8 analysis, a laser‑scanning confocal microscope, and western blot analysis. The results demonstrated that 5% serum exerted a chondroprotective effect more than the other concentrations of serum, as it simultaneously promoted cell proliferation, autophagy, and ECM synthesis in human OA Chondrocytes. Furthermore, the decreased mechanistic target of rapamycin (mTOR) and increased Akt were observed in 5% serum‑treated OA Chondrocytes. Either mTOR or Akt inhibitor influenced the effect of 5% serum on cell proliferation and autophagy in human OA Chondrocytes, which was associated with LC‑3B or B‑cell lymphoma-2 (Bcl‑2) signal molecules. Consistent with previous studies, the present study proposes that 5% serum promotes cell proliferation via the Akt/Bcl‑2 axis and induces autophagy via the mTOR/LC‑3B axis in human OA Chondrocytes. Furthermore, the different roles of Akt and mTOR in the cell processes of human OA Chondrocytes require consideration for preclinical and clinical therapy of OA.
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Different roles of Akt and mechanistic target of rapamycin in serum‑dependent chondroprotection of human osteoarthritic Chondrocytes
International Journal of Molecular Medicine, 2017Co-Authors: Tongen Zhang, Xinpeng Zheng, Bing ZhangAbstract:: Despite various animal serums being used widely to Culture Chondrocytes, the regulatory mechanism of serum on chondrocyte activities has not been elucidated. In the present study, human osteoarthritis (OA) Chondrocytes were used to perform in vitro investigations on the effect of different concentrations of bovine fetal serum on extracellular matrix synthesis, cell proliferation and autophagy using the Cell Counting Kit‑8 analysis, a laser‑scanning confocal microscope, and western blot analysis. The results demonstrated that 5% serum exerted a chondroprotective effect more than the other concentrations of serum, as it simultaneously promoted cell proliferation, autophagy, and ECM synthesis in human OA Chondrocytes. Furthermore, the decreased mechanistic target of rapamycin (mTOR) and increased Akt were observed in 5% serum‑treated OA Chondrocytes. Either mTOR or Akt inhibitor influenced the effect of 5% serum on cell proliferation and autophagy in human OA Chondrocytes, which was associated with LC‑3B or B‑cell lymphoma-2 (Bcl‑2) signal molecules. Consistent with previous studies, the present study proposes that 5% serum promotes cell proliferation via the Akt/Bcl‑2 axis and induces autophagy via the mTOR/LC‑3B axis in human OA Chondrocytes. Furthermore, the different roles of Akt and mTOR in the cell processes of human OA Chondrocytes require consideration for preclinical and clinical therapy of OA.
R. Garrone - One of the best experts on this subject based on the ideXlab platform.
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Proteoglycan core protein and type II collagen gene expressions are not correlated with cell shape changes during low density chondrocyte Cultures.
Differentiation, 1990Co-Authors: F. Mallein-gerin, Florence Ruggiero, R. GarroneAbstract:Chondrocytes isolated from chicken embryo sterna were cultivated in low density monolayer Cultures to induce their dedifferentiation. At different stages of the long-term Cultures, changes in expression of a cartilage-specific sulfated proteoglycan and cartilage-characteristic type II collagen have been examined and related to the shape change of cells using in situ hybridization and immunocytochemistry. At the beginning of the Culture, all cells exhibit a round shape and express the cartilage phenotype. Then, during the course of the Culture, Chondrocytes flatten and become fibroblast-like, but this morphological modification does not start for all the cells at the same time. Interestingly, the loss of cartilage proteoglycan or type II collagen expression did not occur for all polygonal or fibroblast-like cells. Moreover, we observed a variability in the steady state levels of RNA or protein accumulation among Chondrocytes exhibiting a similar shape, as judged by the intensity of hybridization signal or immunofluorescence over the cells. These observations support the hypothesis that the shape change does not have a causative role in the chondrocyte phenotype expression, but is rather a secondary effect of the dedifferentiation process. Furthermore, the disappearance of hybridizable core protein or type II collagen mRNA during the dedifferentiation process was coincident with the disappearance of the proteins for which they code as detected by immunohistochemical staining. This suggest that core protein and type II collagen gene expressions are controlled primarily at the transcriptional level in long-term chondrocyte Cultures.Chondrocytes isolated from chicken embryo sterna were cultivated in low density monolayer Cultures to induce their dedifferentiation. At different stages of the long-term Cultures, changes in expression of a cartilage-specific sulfated proteoglycan and cartilage-characteristic type II collagen have been examined and related to the shape change of cells using in situ hybridization and immunocytochemistry. At the beginning of the Culture, all cells exhibit a round shape and express the cartilage phenotype. Then, during the course of the Culture, Chondrocytes flatten and become fibroblast-like, but this morphological modification does not start for all the cells at the same time. Interestingly, the loss of cartilage proteoglycan or type II collagen expression did not occur for all polygonal or fibroblast-like cells. Moreover, we observed a variability in the steady state levels of RNA or protein accumulation among Chondrocytes exhibiting a similar shape, as judged by the intensity of hybridization signal or immunofluorescence over the cells. These observations support the hypothesis that the shape change does not have a causative role in the chondrocyte phenotype expression, but is rather a secondary effect of the dedifferentiation process. Furthermore, the disappearance of hybridizable core protein or type II collagen mRNA during the dedifferentiation process was coincident with the disappearance of the proteins for which they code as detected by immunohistochemical staining. This suggest that core protein and type II collagen gene expressions are controlled primarily at the transcriptional level in long-term chondrocyte Cultures.
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Proteoglycan core protein and type II collagen gene expressions are not correlated with cell shape changes during low density chondrocyte Cultures
Differentiation, 1990Co-Authors: F. Mallein-gerin, Florence Ruggiero, R. GarroneAbstract:Chondrocytes isolated from chicken embryo sterna were cultivated in low density monolayer Cultures to induce their dedifferentiation. At different stages of the long-term Cultures, changes in expression of a cartilage-specific sulfated proteoglycan and cartilage-characteristic type II collagen have been examined and related to the shape change of cells using in situ hybridization and immunocytochemistry. At the beginning of the Culture, all cells exhibit a round shape and express the cartilage phenotype. Then, during the course of the Culture, Chondrocytes flatten and become fibroblast-like, but this morphological modification does not start for all the cells at the same time. Interestingly, the loss of cartilage proteoglycan or type II collagen expression did not occur for all polygonal or fibroblast-like cells. Moreover, we observed a variability in the steady state levels of RNA or protein accumulation among Chondrocytes exhibiting a similar shape, as judged by the intensity of hybridization signal or immunofluorescence over the cells. These observations support the hypothesis that the shape change does not have a causative role in the chondrocyte phenotype expression, but is rather a secondary effect of the dedifferentiation process. Furthermore, the disappearance of hybridizable core protein or type II collagen mRNA during the dedifferentiation process was coincident with the disappearance of the proteins for which they code as detected by immunohistochemical staining. This suggest that core protein and type II collagen gene expressions are controlled primarily at the transcriptional level in long-term chondrocyte Cultures.
Gunii Im - One of the best experts on this subject based on the ideXlab platform.
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a novel hyaluronate atelocollagen β tcp hydroxyapatite biphasic scaffold for the repair of osteochondral defects in rabbits
Tissue Engineering Part A, 2009Co-Authors: Jongsoo Oh, Il Kyu Park, Baeksun Choi, Gunii ImAbstract:The authors devised a novel biphasic scaffold combining hyaluronic acid and atelocollagen for the chondral phase and combining hydroxyapatite (HA) and β-tricalcium phosphate (β-TCP) for the osseous phase. The biphasic scaffold was fabricated by placing the freeze-dried chondral phase over the HA/β-TCP scaffold prewetted with hyaluronate/atelocollagen solution. Chondrocytes were isolated in 28 rabbits, expanded, injected inside the chondral phase of the biphasic scaffold, and then Cultured in chondrogenic medium. After 2 weeks of in vitro Culture, Chondrocytes had evenly infiltrated inside the chondral phase and produced extracellular matrix. For in vivo study, a large osteochondral defect was made on the patellar groove of the right distal femur and managed using one of the following methods: filling with cell–biphasic scaffold composite (group I); implanting only biphasic scaffold (group II); placing the removed osteochondral fragments back into the defect (group III, positive control); leaving empty (gr...
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A Novel Hyaluronate–Atelocollagen/β-TCP–Hydroxyapatite Biphasic Scaffold for the Repair of Osteochondral Defects in Rabbits
Tissue Engineering Part A, 2009Co-Authors: Jongsoo Oh, Il Kyu Park, Baeksun Choi, Gunii ImAbstract:The authors devised a novel biphasic scaffold combining hyaluronic acid and atelocollagen for the chondral phase and combining hydroxyapatite (HA) and β-tricalcium phosphate (β-TCP) for the osseous phase. The biphasic scaffold was fabricated by placing the freeze-dried chondral phase over the HA/β-TCP scaffold prewetted with hyaluronate/atelocollagen solution. Chondrocytes were isolated in 28 rabbits, expanded, injected inside the chondral phase of the biphasic scaffold, and then Cultured in chondrogenic medium. After 2 weeks of in vitro Culture, Chondrocytes had evenly infiltrated inside the chondral phase and produced extracellular matrix. For in vivo study, a large osteochondral defect was made on the patellar groove of the right distal femur and managed using one of the following methods: filling with cell–biphasic scaffold composite (group I); implanting only biphasic scaffold (group II); placing the removed osteochondral fragments back into the defect (group III, positive control); leaving empty (gr...
Tongen Zhang - One of the best experts on this subject based on the ideXlab platform.
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different roles of akt and mechanistic target of rapamycin in serum dependent chondroprotection of human osteoarthritic Chondrocytes
International Journal of Molecular Medicine, 2017Co-Authors: Tongen Zhang, Xinpeng Zheng, Bing ZhangAbstract:: Despite various animal serums being used widely to Culture Chondrocytes, the regulatory mechanism of serum on chondrocyte activities has not been elucidated. In the present study, human osteoarthritis (OA) Chondrocytes were used to perform in vitro investigations on the effect of different concentrations of bovine fetal serum on extracellular matrix synthesis, cell proliferation and autophagy using the Cell Counting Kit‑8 analysis, a laser‑scanning confocal microscope, and western blot analysis. The results demonstrated that 5% serum exerted a chondroprotective effect more than the other concentrations of serum, as it simultaneously promoted cell proliferation, autophagy, and ECM synthesis in human OA Chondrocytes. Furthermore, the decreased mechanistic target of rapamycin (mTOR) and increased Akt were observed in 5% serum‑treated OA Chondrocytes. Either mTOR or Akt inhibitor influenced the effect of 5% serum on cell proliferation and autophagy in human OA Chondrocytes, which was associated with LC‑3B or B‑cell lymphoma-2 (Bcl‑2) signal molecules. Consistent with previous studies, the present study proposes that 5% serum promotes cell proliferation via the Akt/Bcl‑2 axis and induces autophagy via the mTOR/LC‑3B axis in human OA Chondrocytes. Furthermore, the different roles of Akt and mTOR in the cell processes of human OA Chondrocytes require consideration for preclinical and clinical therapy of OA.
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Different roles of Akt and mechanistic target of rapamycin in serum‑dependent chondroprotection of human osteoarthritic Chondrocytes
International Journal of Molecular Medicine, 2017Co-Authors: Tongen Zhang, Xinpeng Zheng, Bing ZhangAbstract:: Despite various animal serums being used widely to Culture Chondrocytes, the regulatory mechanism of serum on chondrocyte activities has not been elucidated. In the present study, human osteoarthritis (OA) Chondrocytes were used to perform in vitro investigations on the effect of different concentrations of bovine fetal serum on extracellular matrix synthesis, cell proliferation and autophagy using the Cell Counting Kit‑8 analysis, a laser‑scanning confocal microscope, and western blot analysis. The results demonstrated that 5% serum exerted a chondroprotective effect more than the other concentrations of serum, as it simultaneously promoted cell proliferation, autophagy, and ECM synthesis in human OA Chondrocytes. Furthermore, the decreased mechanistic target of rapamycin (mTOR) and increased Akt were observed in 5% serum‑treated OA Chondrocytes. Either mTOR or Akt inhibitor influenced the effect of 5% serum on cell proliferation and autophagy in human OA Chondrocytes, which was associated with LC‑3B or B‑cell lymphoma-2 (Bcl‑2) signal molecules. Consistent with previous studies, the present study proposes that 5% serum promotes cell proliferation via the Akt/Bcl‑2 axis and induces autophagy via the mTOR/LC‑3B axis in human OA Chondrocytes. Furthermore, the different roles of Akt and mTOR in the cell processes of human OA Chondrocytes require consideration for preclinical and clinical therapy of OA.
F. Mallein-gerin - One of the best experts on this subject based on the ideXlab platform.
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Proteoglycan core protein and type II collagen gene expressions are not correlated with cell shape changes during low density chondrocyte Cultures.
Differentiation, 1990Co-Authors: F. Mallein-gerin, Florence Ruggiero, R. GarroneAbstract:Chondrocytes isolated from chicken embryo sterna were cultivated in low density monolayer Cultures to induce their dedifferentiation. At different stages of the long-term Cultures, changes in expression of a cartilage-specific sulfated proteoglycan and cartilage-characteristic type II collagen have been examined and related to the shape change of cells using in situ hybridization and immunocytochemistry. At the beginning of the Culture, all cells exhibit a round shape and express the cartilage phenotype. Then, during the course of the Culture, Chondrocytes flatten and become fibroblast-like, but this morphological modification does not start for all the cells at the same time. Interestingly, the loss of cartilage proteoglycan or type II collagen expression did not occur for all polygonal or fibroblast-like cells. Moreover, we observed a variability in the steady state levels of RNA or protein accumulation among Chondrocytes exhibiting a similar shape, as judged by the intensity of hybridization signal or immunofluorescence over the cells. These observations support the hypothesis that the shape change does not have a causative role in the chondrocyte phenotype expression, but is rather a secondary effect of the dedifferentiation process. Furthermore, the disappearance of hybridizable core protein or type II collagen mRNA during the dedifferentiation process was coincident with the disappearance of the proteins for which they code as detected by immunohistochemical staining. This suggest that core protein and type II collagen gene expressions are controlled primarily at the transcriptional level in long-term chondrocyte Cultures.Chondrocytes isolated from chicken embryo sterna were cultivated in low density monolayer Cultures to induce their dedifferentiation. At different stages of the long-term Cultures, changes in expression of a cartilage-specific sulfated proteoglycan and cartilage-characteristic type II collagen have been examined and related to the shape change of cells using in situ hybridization and immunocytochemistry. At the beginning of the Culture, all cells exhibit a round shape and express the cartilage phenotype. Then, during the course of the Culture, Chondrocytes flatten and become fibroblast-like, but this morphological modification does not start for all the cells at the same time. Interestingly, the loss of cartilage proteoglycan or type II collagen expression did not occur for all polygonal or fibroblast-like cells. Moreover, we observed a variability in the steady state levels of RNA or protein accumulation among Chondrocytes exhibiting a similar shape, as judged by the intensity of hybridization signal or immunofluorescence over the cells. These observations support the hypothesis that the shape change does not have a causative role in the chondrocyte phenotype expression, but is rather a secondary effect of the dedifferentiation process. Furthermore, the disappearance of hybridizable core protein or type II collagen mRNA during the dedifferentiation process was coincident with the disappearance of the proteins for which they code as detected by immunohistochemical staining. This suggest that core protein and type II collagen gene expressions are controlled primarily at the transcriptional level in long-term chondrocyte Cultures.
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Proteoglycan core protein and type II collagen gene expressions are not correlated with cell shape changes during low density chondrocyte Cultures
Differentiation, 1990Co-Authors: F. Mallein-gerin, Florence Ruggiero, R. GarroneAbstract:Chondrocytes isolated from chicken embryo sterna were cultivated in low density monolayer Cultures to induce their dedifferentiation. At different stages of the long-term Cultures, changes in expression of a cartilage-specific sulfated proteoglycan and cartilage-characteristic type II collagen have been examined and related to the shape change of cells using in situ hybridization and immunocytochemistry. At the beginning of the Culture, all cells exhibit a round shape and express the cartilage phenotype. Then, during the course of the Culture, Chondrocytes flatten and become fibroblast-like, but this morphological modification does not start for all the cells at the same time. Interestingly, the loss of cartilage proteoglycan or type II collagen expression did not occur for all polygonal or fibroblast-like cells. Moreover, we observed a variability in the steady state levels of RNA or protein accumulation among Chondrocytes exhibiting a similar shape, as judged by the intensity of hybridization signal or immunofluorescence over the cells. These observations support the hypothesis that the shape change does not have a causative role in the chondrocyte phenotype expression, but is rather a secondary effect of the dedifferentiation process. Furthermore, the disappearance of hybridizable core protein or type II collagen mRNA during the dedifferentiation process was coincident with the disappearance of the proteins for which they code as detected by immunohistochemical staining. This suggest that core protein and type II collagen gene expressions are controlled primarily at the transcriptional level in long-term chondrocyte Cultures.
