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Shinsuke Ohba - One of the best experts on this subject based on the ideXlab platform.
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Gli1 Haploinsufficiency Leads to Decreased Bone Mass with an Uncoupling of Bone Metabolism in Adult Mice
PloS one, 2014Co-Authors: Yoshiaki Kitaura, Hironori Hojo, Yuske Komiyama, Tsuyoshi Takato, Ung-il Chung, Shinsuke OhbaAbstract:Hedgehog (Hh) signaling plays important roles in various development processes. This signaling is necessary for osteoblast formation during endochondral ossification. In contrast to the established roles of Hh signaling in embryonic Bone formation, evidence of its roles in adult Bone homeostasis is not complete. Here we report the involvement of Gli1, a transcriptional activator induced by Hh signaling activation, in postnatal Bone homeostasis under physiological and pathological conditions. Skeletal analyses of Gli1+/− adult mice revealed that Gli1 haploinsufficiency caused decreased Bone mass with reduced Bone formation and accelerated Bone resorption, suggesting an uncoupling of Bone Metabolism. Hh-mediated osteoblast differentiation was largely impaired in cultures of Gli1+/− precursors, and the impairment was rescued by Gli1 expression via adenoviral transduction. In addition, Gli1+/− precursors showed premature differentiation into osteocytes and increased ability to support osteoclastogenesis. When we compared fracture healing between wild-type and Gli1+/− adult mice, we found that the Gli1+/− mice exhibited impaired fracture healing with insufficient soft callus formation. These data suggest that Gli1, acting downstream of Hh signaling, contributes to adult Bone Metabolism, in which this molecule not only promotes osteoblast differentiation but also represses osteoblast maturation toward osteocytes to maintain normal Bone homeostasis.
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Gli1 Haploinsufficiency Leads to Decreased Bone Mass with an Uncoupling of Bone Metabolism in Adult Mice
2014Co-Authors: Yoshiaki Kitaura, Hironori Hojo, Yuske Komiyama, Tsuyoshi Takato, Ung-il Chung, Shinsuke OhbaAbstract:Hedgehog (Hh) signaling plays important roles in various development processes. This signaling is necessary for osteoblast formation during endochondral ossification. In contrast to the established roles of Hh signaling in embryonic Bone formation, evidence of its roles in adult Bone homeostasis is not complete. Here we report the involvement of Gli1, a transcriptional activator induced by Hh signaling activation, in postnatal Bone homeostasis under physiological and pathological conditions. Skeletal analyses of Gli1+/2 adult mice revealed that Gli1 haploinsufficiency caused decreased Bone mass with reduced Bone formation and accelerated Bone resorption, suggesting an uncoupling of Bone Metabolism. Hh-mediated osteoblast differentiation was largely impaired in cultures of Gli1+/2 precursors, and the impairment was rescued by Gli1 expression via adenoviral transduction. In addition, Gli1+/2 precursors showed premature differentiation into osteocytes and increased ability to support osteoclastogenesis. When we compared fracture healing between wild-type and Gli1+/2 adult mice, we found that the Gli1+/2mice exhibited impaired fracture healing with insufficient soft callus formation. These data suggest that Gli1, acting downstream of Hh signaling, contributes to adult Bone Metabolism, in which this molecule not only promotes osteoblast differentiation but also represses osteoblast maturation toward osteocytes t
Mingsheng Tan - One of the best experts on this subject based on the ideXlab platform.
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15 deoxy δ 12 14 prostaglandin j 2 as a potential regulator of Bone Metabolism via pparγ dependent and independent pathways a review
Drug Design Development and Therapy, 2019Co-Authors: Zhencheng Xiong, Pan Luo, Jun Zhou, Mingsheng TanAbstract:Bone Metabolism is a complex physiological process that primarily involves osteoblast-mediated Bone formation and osteoclast-mediated Bone resorption, both of which are regulated by a variety of biological factors. There is increasing evidence that peroxisome proliferator-activated receptor γ (PPARγ) is a member of the nuclear receptor superfamily and plays an important role in lipid Metabolism and Bone Metabolism. Through the PPARγ-dependent pathway, 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) promotes the formation of marrow adipocytes and inhibits the formation of osteoblasts, resulting in Bone loss and increasing the risk of fracture and osteoporosis. Recent studies have found that through the PPARγ-independent pathway, 15d-PGJ2 plays a regulatory role in Bone metastasis of breast cancer, which can inhibit osteoclastogenesis and reduce Bone destruction. The purpose of our review is to summarize the recent progress in elucidating the mechanisms and effects of 15d-PGJ2 in Bone Metabolism, which can serve as a novel therapeutic target for Bone tumors, osteoporosis, rheumatoid arthritis (RA), and other Bone diseases.
Christel Lambergallardt - One of the best experts on this subject based on the ideXlab platform.
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acute effects of calcium carbonate calcium citrate and potassium citrate on markers of calcium and Bone Metabolism in young women
British Journal of Nutrition, 2009Co-Authors: Heini Karp, Maarit E. Ketola, Christel LambergallardtAbstract:Both K and Ca supplementation may have beneficial effects on Bone through separate mechanisms. K in the form of citrate or bicarbonate affects Bone by neutralising the acid load caused by a high protein intake or a low intake of alkalising foods, i.e. fruits and vegetables. Ca is known to decrease serum parathyroid hormone (S-PTH) concentration and Bone resorption. We compared the effects of calcium carbonate, calcium citrate and potassium citrate on markers of Ca and Bone Metabolism in young women. Twelve healthy women aged 22‐ 30 years were randomised into four controlled 24 h study sessions, each subject serving as her own control. At the beginning of each session, subjects received a single dose of calcium carbonate, calcium citrate, potassium citrate or a placebo in randomised order. The diet during each session was identical, containing 300 mg Ca. Both the calcium carbonate and calcium citrate supplement contained 1000 mg Ca; the potassium citrate supplement contained 2250 mg K. Markers of Ca and Bone Metabolism were followed. Potassium citrate decreased the Bone resorption marker (N-terminal telopeptide of type I collagen) and increased Ca retention relative to the control session. Both Ca supplements decreased S-PTH concentration. Ca supplements also decreased Bone resorption relative to the control session, but this was significant only for calcium carbonate. No differences in Bone formation marker (Bone-specific alkaline phosphatase) were seen among the study sessions. The results suggest that potassium citrate has a positive effect on the resorption marker despite low Ca intake. Both Ca supplements were absorbed well and decreased S-PTH efficiently. Calcium: Potassium: Acid–base homeostasis: Bone Metabolism
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high phosphorus intakes acutely and negatively affect ca and Bone Metabolism in a dose dependent manner in healthy young females
British Journal of Nutrition, 2006Co-Authors: Virpi Kemi, Merja Karkkainen, Christel LambergallardtAbstract:Ca and P are both essential nutrients for Bone and are known to affect one of the most important regulators of Bone Metabolism, parathyroid hormone (PTH). Too ample a P intake, typical of Western diets, could be deleterious to Bone through the increased PTH secretion. Few controlled dose-response studies are available on the effects of high P intake in man. We studied the short-term effects of four P doses on Ca and Bone Metabolism in fourteen healthy women, 20-28 years of age, who were randomized to four controlled study days; thus each study subject served as her own control. P supplement doses of 0 (placebo), 250, 750 or 1500 mg were taken, divided into three doses during the study day. The meals served were exactly the same during each study day and provided 495 mg P and 250 mg Ca. The P doses affected the serum PTH (S-PTH) in a dose-dependent manner (P=0.0005). There was a decrease in serum ionized Ca concentration only in the highest P dose (P=0.004). The marker of Bone formation, Bone-specific alkaline phosphatase, decreased (P=0.05) and the Bone resorption marker, N-terminal telopeptide of collagen type I, increased in response to the P doses (P=0.05). This controlled dose-response study showed that P has a dose-dependent effect on S-PTH and increases PTH secretion significantly when Ca intake is low. Acutely high P intake adversely affects Bone Metabolism by decreasing Bone formation and increasing Bone resorption, as indicated by the Bone Metabolism markers.
Yoshiaki Kitaura - One of the best experts on this subject based on the ideXlab platform.
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Gli1 Haploinsufficiency Leads to Decreased Bone Mass with an Uncoupling of Bone Metabolism in Adult Mice
PloS one, 2014Co-Authors: Yoshiaki Kitaura, Hironori Hojo, Yuske Komiyama, Tsuyoshi Takato, Ung-il Chung, Shinsuke OhbaAbstract:Hedgehog (Hh) signaling plays important roles in various development processes. This signaling is necessary for osteoblast formation during endochondral ossification. In contrast to the established roles of Hh signaling in embryonic Bone formation, evidence of its roles in adult Bone homeostasis is not complete. Here we report the involvement of Gli1, a transcriptional activator induced by Hh signaling activation, in postnatal Bone homeostasis under physiological and pathological conditions. Skeletal analyses of Gli1+/− adult mice revealed that Gli1 haploinsufficiency caused decreased Bone mass with reduced Bone formation and accelerated Bone resorption, suggesting an uncoupling of Bone Metabolism. Hh-mediated osteoblast differentiation was largely impaired in cultures of Gli1+/− precursors, and the impairment was rescued by Gli1 expression via adenoviral transduction. In addition, Gli1+/− precursors showed premature differentiation into osteocytes and increased ability to support osteoclastogenesis. When we compared fracture healing between wild-type and Gli1+/− adult mice, we found that the Gli1+/− mice exhibited impaired fracture healing with insufficient soft callus formation. These data suggest that Gli1, acting downstream of Hh signaling, contributes to adult Bone Metabolism, in which this molecule not only promotes osteoblast differentiation but also represses osteoblast maturation toward osteocytes to maintain normal Bone homeostasis.
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Gli1 Haploinsufficiency Leads to Decreased Bone Mass with an Uncoupling of Bone Metabolism in Adult Mice
2014Co-Authors: Yoshiaki Kitaura, Hironori Hojo, Yuske Komiyama, Tsuyoshi Takato, Ung-il Chung, Shinsuke OhbaAbstract:Hedgehog (Hh) signaling plays important roles in various development processes. This signaling is necessary for osteoblast formation during endochondral ossification. In contrast to the established roles of Hh signaling in embryonic Bone formation, evidence of its roles in adult Bone homeostasis is not complete. Here we report the involvement of Gli1, a transcriptional activator induced by Hh signaling activation, in postnatal Bone homeostasis under physiological and pathological conditions. Skeletal analyses of Gli1+/2 adult mice revealed that Gli1 haploinsufficiency caused decreased Bone mass with reduced Bone formation and accelerated Bone resorption, suggesting an uncoupling of Bone Metabolism. Hh-mediated osteoblast differentiation was largely impaired in cultures of Gli1+/2 precursors, and the impairment was rescued by Gli1 expression via adenoviral transduction. In addition, Gli1+/2 precursors showed premature differentiation into osteocytes and increased ability to support osteoclastogenesis. When we compared fracture healing between wild-type and Gli1+/2 adult mice, we found that the Gli1+/2mice exhibited impaired fracture healing with insufficient soft callus formation. These data suggest that Gli1, acting downstream of Hh signaling, contributes to adult Bone Metabolism, in which this molecule not only promotes osteoblast differentiation but also represses osteoblast maturation toward osteocytes t
Zhencheng Xiong - One of the best experts on this subject based on the ideXlab platform.
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15 deoxy δ 12 14 prostaglandin j 2 as a potential regulator of Bone Metabolism via pparγ dependent and independent pathways a review
Drug Design Development and Therapy, 2019Co-Authors: Zhencheng Xiong, Pan Luo, Jun Zhou, Mingsheng TanAbstract:Bone Metabolism is a complex physiological process that primarily involves osteoblast-mediated Bone formation and osteoclast-mediated Bone resorption, both of which are regulated by a variety of biological factors. There is increasing evidence that peroxisome proliferator-activated receptor γ (PPARγ) is a member of the nuclear receptor superfamily and plays an important role in lipid Metabolism and Bone Metabolism. Through the PPARγ-dependent pathway, 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) promotes the formation of marrow adipocytes and inhibits the formation of osteoblasts, resulting in Bone loss and increasing the risk of fracture and osteoporosis. Recent studies have found that through the PPARγ-independent pathway, 15d-PGJ2 plays a regulatory role in Bone metastasis of breast cancer, which can inhibit osteoclastogenesis and reduce Bone destruction. The purpose of our review is to summarize the recent progress in elucidating the mechanisms and effects of 15d-PGJ2 in Bone Metabolism, which can serve as a novel therapeutic target for Bone tumors, osteoporosis, rheumatoid arthritis (RA), and other Bone diseases.