The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform
Huayue Chen - One of the best experts on this subject based on the ideXlab platform.
-
Segmental variations in trabecular bone density and microstructure of the spine in senescence-accelerated mouse (SAMP6): A murine model for Senile Osteoporosis ☆
Experimental gerontology, 2012Co-Authors: Huayue Chen, Kin-ya KuboAbstract:The senescence-accelerated mouse strain P6 (SAMP6) is a model of Senile Osteoporosis, which possesses many features of Senile Osteoporosis in humans. So far, little is known about the systemic bone microstructural changes that occur at the cervical, thoracic, and lumbar vertebrae. In this study, we therefore investigated segmental variations of vertebral trabecular bone mineral density (BMD) and three-dimensional microstructure in SAMP6 and the normal control mouse (SAMR1) at 12 months of age using quantitative micro computed tomography (micro-CT) and image analysis software. The vertebral height and vertebral cross-sectional area (CSA) increased, while vertebral trabecular BMD and trabecular bone volume fraction (BV/TV) decreased from the cervical to lumbar spine both in SAMR1 and SAMP6. As compared with SAMR1, the thoracic vertebral CSA had a tendency to be low and the lumbar vertebral CSA was significantly declined in SAMP6. The vertebral trabecular BMD, BV/TV, trabecular thickness (Tb.Th), and trabecular number (Tb.N) significantly decreased in cervical, thoracic and lumbar spine of SAMP6. Trabecular bone pattern factor (TBPf) was higher at the lumbar spine and the structure model index (SMI) of the lower thoracic and lumbar spine was higher in SAMP6. These results indicate that vertebral trabecular bone microstructures are remarkably heterogeneous throughout the spine in both SAMR1 and SAMP6. The decrease of vertebral trabecular bone density in SAMP6 advanced faster caudally than cranially within the spine, similar phenomena were observed in humans. These findings highlight the relevance of SAMP6 for studies of vertebral fragility associated with Senile Osteoporosis.
-
site specific bone loss in senescence accelerated mouse samp6 a murine model for Senile Osteoporosis
Experimental Gerontology, 2009Co-Authors: Huayue Chen, Xiangrong Zhou, Shoichi Emura, Shizuko ShoumuraAbstract:The senescence-accelerated mouse strain P6 (SAMP6) is a model of Senile Osteoporosis, which possesses many features of Senile Osteoporosis in humans. So far, little is known about the systemic bone microstructural changes that occur at multiple skeletal sites. In this study, we therefore, investigated site (vertebra, femur and tibia) dependence of bone microstructure and bone mineral density (BMD) in SAMP6 and the normal control mouse (SAMR1) at 5 and 12 months of age using quantitative micro computed tomography (micro-CT) and image analysis software. As compared with SAMR1, the most prominent change in SAMP6 was the reduction of vertebral trabecular bone volume fraction (BV/TV) and trabecular BMD. Moderate decrease of trabecular bone mass was observed in the proximal tibia and distal femur. Increased marrow area and periosteal perimeter were investigated, though the cortical area and cortical thickness had no marked changes in the mid-tibial and mid-femoral cortical bones. These results indicate that bone microstructural properties in SAMP6 are remarkably heterogeneous throughout the skeleton, which is analogous to changes that occur in human bones. These findings further validate the relevance of SAMP6 as a model of Senile Osteoporosis.
-
ultrastructural changes in bones of the senescence accelerated mouse samp6 a murine model for Senile Osteoporosis
Histology and Histopathology, 2004Co-Authors: Huayue Chen, Shizuko Shoumura, Shoichi EmuraAbstract:SAMP6, a substrain of senescenceaccelerated mice, was developed as an animal model for Senile Osteoporosis. In the present study, we investigated the bone morphology, together with serum calcium and bone mineral density (BMD) in SAMP6 and agematched normal mice SAMR1. We did not find any significant differences between SAMR1 and SAMP6 at 1 month of age with regard to the serum compositions and bone morphology. As compared with SAMR1, BMD, the femoral weight, femoral calcium and phosphorus levels were significantly reduced in SAMP6 at 2 and 5 months of age. The number of osteoblasts in trabecular bones was also significantly reduced. Swollen mitochondria and myelin-like structures were found in osteoblasts and osteocytes of SAMP6 mice at 2 and 5 months of age. There was a greater proportion of resting surface and less forming surface in the femoral endosteal surfaces of SAMP6 mice. The amount of trabecular bone in the lumbar vertebra and the distal metaphysis of the femur was reduced. The number of the mast cells in bone marrow of the tibia significantly increased in SAMP6 mice. These findings indicate that the lower bone mass in SAMP6 was due to the reduction in osteoblast formation and suggested that mast cells in bone marrows play a role in the pathogenesis of Senile Osteoporosis.
Kin-ya Kubo - One of the best experts on this subject based on the ideXlab platform.
-
Morphological and molecular characterization of the Senile Osteoporosis in senescence-accelerated mouse prone 6 (SAMP6)
Medical Molecular Morphology, 2018Co-Authors: Kagaku Azuma, Qian Zhou, Kin-ya KuboAbstract:Although the understanding of the complex pathogenesis for Osteoporosis is appreciable, the underlying mechanism is not yet fully elucidated. There is a great need to further characterize the available animal models in Osteoporosis research. The senescence-accelerated mouse prone 6 (SAMP6) mice have been developed as the spontaneous experimental model for Senile Osteoporosis. Here, we provide a comprehensive overview of current research regarding the bone morphological and molecular alterations and the possible mechanisms involved in these changes. There were significant decrease in trabecular bone mass at the axial and appendicular skeletal sites, with no marked alterations of cortical bone. Decreased bone formation on the endosteal surface and trabecular bone, and increased bone marrow adiposity were observed in SAMP6 mice. The elevated expression level of proliferator activator gamma (PPARγ) in the bone marrow suggest that PPARγ might regulate osteoblastic bone formation negatively in SAMP6 mice. The expression level of secreted frizzled-related protein 4 (Sfrp4) was found to be higher in SAMP6 mice. Sfrp4 is considered to suppress osteoblastic proliferation mediated by inhibition of Wnt signaling pathway. These findings may help us to gain more insight into the potential mechanism of Senile Osteoporosis.
-
Segmental variations in trabecular bone density and microstructure of the spine in senescence-accelerated mouse (SAMP6): A murine model for Senile Osteoporosis ☆
Experimental gerontology, 2012Co-Authors: Huayue Chen, Kin-ya KuboAbstract:The senescence-accelerated mouse strain P6 (SAMP6) is a model of Senile Osteoporosis, which possesses many features of Senile Osteoporosis in humans. So far, little is known about the systemic bone microstructural changes that occur at the cervical, thoracic, and lumbar vertebrae. In this study, we therefore investigated segmental variations of vertebral trabecular bone mineral density (BMD) and three-dimensional microstructure in SAMP6 and the normal control mouse (SAMR1) at 12 months of age using quantitative micro computed tomography (micro-CT) and image analysis software. The vertebral height and vertebral cross-sectional area (CSA) increased, while vertebral trabecular BMD and trabecular bone volume fraction (BV/TV) decreased from the cervical to lumbar spine both in SAMR1 and SAMP6. As compared with SAMR1, the thoracic vertebral CSA had a tendency to be low and the lumbar vertebral CSA was significantly declined in SAMP6. The vertebral trabecular BMD, BV/TV, trabecular thickness (Tb.Th), and trabecular number (Tb.N) significantly decreased in cervical, thoracic and lumbar spine of SAMP6. Trabecular bone pattern factor (TBPf) was higher at the lumbar spine and the structure model index (SMI) of the lower thoracic and lumbar spine was higher in SAMP6. These results indicate that vertebral trabecular bone microstructures are remarkably heterogeneous throughout the spine in both SAMR1 and SAMP6. The decrease of vertebral trabecular bone density in SAMP6 advanced faster caudally than cranially within the spine, similar phenomena were observed in humans. These findings highlight the relevance of SAMP6 for studies of vertebral fragility associated with Senile Osteoporosis.
Shizuko Shoumura - One of the best experts on this subject based on the ideXlab platform.
-
site specific bone loss in senescence accelerated mouse samp6 a murine model for Senile Osteoporosis
Experimental Gerontology, 2009Co-Authors: Huayue Chen, Xiangrong Zhou, Shoichi Emura, Shizuko ShoumuraAbstract:The senescence-accelerated mouse strain P6 (SAMP6) is a model of Senile Osteoporosis, which possesses many features of Senile Osteoporosis in humans. So far, little is known about the systemic bone microstructural changes that occur at multiple skeletal sites. In this study, we therefore, investigated site (vertebra, femur and tibia) dependence of bone microstructure and bone mineral density (BMD) in SAMP6 and the normal control mouse (SAMR1) at 5 and 12 months of age using quantitative micro computed tomography (micro-CT) and image analysis software. As compared with SAMR1, the most prominent change in SAMP6 was the reduction of vertebral trabecular bone volume fraction (BV/TV) and trabecular BMD. Moderate decrease of trabecular bone mass was observed in the proximal tibia and distal femur. Increased marrow area and periosteal perimeter were investigated, though the cortical area and cortical thickness had no marked changes in the mid-tibial and mid-femoral cortical bones. These results indicate that bone microstructural properties in SAMP6 are remarkably heterogeneous throughout the skeleton, which is analogous to changes that occur in human bones. These findings further validate the relevance of SAMP6 as a model of Senile Osteoporosis.
-
ultrastructural changes in bones of the senescence accelerated mouse samp6 a murine model for Senile Osteoporosis
Histology and Histopathology, 2004Co-Authors: Huayue Chen, Shizuko Shoumura, Shoichi EmuraAbstract:SAMP6, a substrain of senescenceaccelerated mice, was developed as an animal model for Senile Osteoporosis. In the present study, we investigated the bone morphology, together with serum calcium and bone mineral density (BMD) in SAMP6 and agematched normal mice SAMR1. We did not find any significant differences between SAMR1 and SAMP6 at 1 month of age with regard to the serum compositions and bone morphology. As compared with SAMR1, BMD, the femoral weight, femoral calcium and phosphorus levels were significantly reduced in SAMP6 at 2 and 5 months of age. The number of osteoblasts in trabecular bones was also significantly reduced. Swollen mitochondria and myelin-like structures were found in osteoblasts and osteocytes of SAMP6 mice at 2 and 5 months of age. There was a greater proportion of resting surface and less forming surface in the femoral endosteal surfaces of SAMP6 mice. The amount of trabecular bone in the lumbar vertebra and the distal metaphysis of the femur was reduced. The number of the mast cells in bone marrow of the tibia significantly increased in SAMP6 mice. These findings indicate that the lower bone mass in SAMP6 was due to the reduction in osteoblast formation and suggested that mast cells in bone marrows play a role in the pathogenesis of Senile Osteoporosis.
Shoichi Emura - One of the best experts on this subject based on the ideXlab platform.
-
site specific bone loss in senescence accelerated mouse samp6 a murine model for Senile Osteoporosis
Experimental Gerontology, 2009Co-Authors: Huayue Chen, Xiangrong Zhou, Shoichi Emura, Shizuko ShoumuraAbstract:The senescence-accelerated mouse strain P6 (SAMP6) is a model of Senile Osteoporosis, which possesses many features of Senile Osteoporosis in humans. So far, little is known about the systemic bone microstructural changes that occur at multiple skeletal sites. In this study, we therefore, investigated site (vertebra, femur and tibia) dependence of bone microstructure and bone mineral density (BMD) in SAMP6 and the normal control mouse (SAMR1) at 5 and 12 months of age using quantitative micro computed tomography (micro-CT) and image analysis software. As compared with SAMR1, the most prominent change in SAMP6 was the reduction of vertebral trabecular bone volume fraction (BV/TV) and trabecular BMD. Moderate decrease of trabecular bone mass was observed in the proximal tibia and distal femur. Increased marrow area and periosteal perimeter were investigated, though the cortical area and cortical thickness had no marked changes in the mid-tibial and mid-femoral cortical bones. These results indicate that bone microstructural properties in SAMP6 are remarkably heterogeneous throughout the skeleton, which is analogous to changes that occur in human bones. These findings further validate the relevance of SAMP6 as a model of Senile Osteoporosis.
-
ultrastructural changes in bones of the senescence accelerated mouse samp6 a murine model for Senile Osteoporosis
Histology and Histopathology, 2004Co-Authors: Huayue Chen, Shizuko Shoumura, Shoichi EmuraAbstract:SAMP6, a substrain of senescenceaccelerated mice, was developed as an animal model for Senile Osteoporosis. In the present study, we investigated the bone morphology, together with serum calcium and bone mineral density (BMD) in SAMP6 and agematched normal mice SAMR1. We did not find any significant differences between SAMR1 and SAMP6 at 1 month of age with regard to the serum compositions and bone morphology. As compared with SAMR1, BMD, the femoral weight, femoral calcium and phosphorus levels were significantly reduced in SAMP6 at 2 and 5 months of age. The number of osteoblasts in trabecular bones was also significantly reduced. Swollen mitochondria and myelin-like structures were found in osteoblasts and osteocytes of SAMP6 mice at 2 and 5 months of age. There was a greater proportion of resting surface and less forming surface in the femoral endosteal surfaces of SAMP6 mice. The amount of trabecular bone in the lumbar vertebra and the distal metaphysis of the femur was reduced. The number of the mast cells in bone marrow of the tibia significantly increased in SAMP6 mice. These findings indicate that the lower bone mass in SAMP6 was due to the reduction in osteoblast formation and suggested that mast cells in bone marrows play a role in the pathogenesis of Senile Osteoporosis.
Akinori Hishiya - One of the best experts on this subject based on the ideXlab platform.
-
Mouse models of Senile Osteoporosis.
Molecular aspects of medicine, 2005Co-Authors: Ken Watanabe, Akinori HishiyaAbstract:Little is known about the pathophysiology of normal human and mouse senescence. On the other hand, the pathology of age-related disorders, such as Senile Osteoporosis, has been investigated. In vivo studies on the pathology of Osteoporosis have been conducted primarily in rodents. Although mouse models of Senile Osteoporosis display some discrepancies relative to their human counterparts with regard to symptoms and pathology, these experimental models are useful and powerful tools for basic and preclinical studies. Here, we review existing mouse models of Senile Osteoporosis, including those exhibiting premature aging phenotypes, and discuss their pathogenesis, particularly with regard to age-related changes in stem cells.
-
Progeroid syndrome as a model for impaired bone formation in Senile Osteoporosis
Journal of Bone and Mineral Metabolism, 2004Co-Authors: Akinori Hishiya, Ken WatanabeAbstract:Senile or age-related/dependent Osteoporosis is caused by reduced bone formation, rather than increased bone resorption as in postmenopausal Osteoporosis. Here we review genetically engineered mouse models with defects in osteoblastic proliferation or differentiation with focus on IGF signaling and stem cells. Model mice for human progeroid syndromes may provide useful tools for studying the pathogenesis of Senile Osteoporosis.
