The Experts below are selected from a list of 161829 Experts worldwide ranked by ideXlab platform
Yuki Matsushita - One of the best experts on this subject based on the ideXlab platform.
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Skeletal Stem Cells for Bone Development and Repair: Diversity Matters.
Current Osteoporosis Reports, 2020Co-Authors: Yuki Matsushita, Wanida Ono, Noriaki OnoAbstract:Skeletal stem cells (SSCs) are considered to play important roles in Bone Development and repair. These cells have been historically defined by their in vitro potential for self-renewal and differentiation into “trilineage” cells; however, little is known about their in vivo identity. Here, we discuss recent progress on SSCs and how they potentially contribute to Bone Development and repair. Bone is composed of diverse tissues, which include cartilage and its perichondrium, cortical Bone and its periosteum, and Bone marrow and its trabecular Bone and stromal compartment. We are now at the initial stage of understanding the precise identity of SSCs in each Bone tissue. The emerging concept is that functionally dedicated SSCs are encased by their own unique cellular and extracellular matrix microenvironment, and locally support its own compartment. Diverse groups of SSCs are likely to work in concert to achieve Development and repair of the highly functional skeletal organ.
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Skeletal Stem Cells for Bone Development and Repair: Diversity Matters
Current Osteoporosis Reports, 2020Co-Authors: Yuki MatsushitaAbstract:Purpose of Review Skeletal stem cells (SSCs) are considered to play important roles in Bone Development and repair. These cells have been historically defined by their in vitro potential for self-renewal and differentiation into “trilineage” cells; however, little is known about their in vivo identity. Here, we discuss recent progress on SSCs and how they potentially contribute to Bone Development and repair. Recent Findings Bone is composed of diverse tissues, which include cartilage and its perichondrium, cortical Bone and its periosteum, and Bone marrow and its trabecular Bone and stromal compartment. We are now at the initial stage of understanding the precise identity of SSCs in each Bone tissue. The emerging concept is that functionally dedicated SSCs are encased by their own unique cellular and extracellular matrix microenvironment, and locally support its own compartment. Summary Diverse groups of SSCs are likely to work in concert to achieve Development and repair of the highly functional skeletal organ.
Michael T. Longaker - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms of Bone Development and repair
Nature Reviews Molecular Cell Biology, 2020Co-Authors: Ankit Salhotra, Harsh N. Shah, Benjamin Levi, Michael T. LongakerAbstract:This Review discusses the cell types, critical genes and transcription factors involved in Bone Development and repair. The dysfunctional cellular and molecular signalling that results in clinical Bone disease is also outlined, thus informing the current state of science and clinical practice. Bone Development occurs through a series of synchronous events that result in the formation of the body scaffold. The repair potential of Bone and its surrounding microenvironment — including inflammatory, endothelial and Schwann cells — persists throughout adulthood, enabling restoration of tissue to its homeostatic functional state. The isolation of a single skeletal stem cell population through cell surface markers and the Development of single-cell technologies are enabling precise elucidation of cellular activity and fate during Bone repair by providing key insights into the mechanisms that maintain and regenerate Bone during homeostasis and repair. Increased understanding of Bone Development, as well as normal and aberrant Bone repair, has important therapeutic implications for the treatment of Bone disease and ageing-related degeneration.
Ankit Salhotra - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms of Bone Development and repair
Nature Reviews Molecular Cell Biology, 2020Co-Authors: Ankit Salhotra, Harsh N. Shah, Benjamin Levi, Michael T. LongakerAbstract:This Review discusses the cell types, critical genes and transcription factors involved in Bone Development and repair. The dysfunctional cellular and molecular signalling that results in clinical Bone disease is also outlined, thus informing the current state of science and clinical practice. Bone Development occurs through a series of synchronous events that result in the formation of the body scaffold. The repair potential of Bone and its surrounding microenvironment — including inflammatory, endothelial and Schwann cells — persists throughout adulthood, enabling restoration of tissue to its homeostatic functional state. The isolation of a single skeletal stem cell population through cell surface markers and the Development of single-cell technologies are enabling precise elucidation of cellular activity and fate during Bone repair by providing key insights into the mechanisms that maintain and regenerate Bone during homeostasis and repair. Increased understanding of Bone Development, as well as normal and aberrant Bone repair, has important therapeutic implications for the treatment of Bone disease and ageing-related degeneration.
Toshihisa Komori - One of the best experts on this subject based on the ideXlab platform.
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signaling networks in runx2 dependent Bone Development
Journal of Cellular Biochemistry, 2011Co-Authors: Toshihisa KomoriAbstract:RUNX2 is an essential transcription factor for osteoblast differentiation and chondrocyte maturation. SP7, another transcription factor, is required for osteoblast differentiation. Major signaling pathways, including FGF, Wnt, and IHH, also play important roles in skeletal Development. RUNX2 regulates Sp7 expression at an early stage of osteoblast differentiation. FGF2 upregulates Runx2 expression and activates RUNX2, and gain-of-function mutations of FGFRs cause craniosynostosis and limb defect with upregulation of Runx2 expression. Wnt signaling upregulates Runx2 expression and activates RUNX2, and RUNX2 induces Tcf7 expression. IHH is required for Runx2 expression in osteoprogenitor cells during endochondral Bone Development, and RUNX2 directly regulates Ihh expression in chondrocytes. Thus, RUNX2 regulates osteoblast differentiation and chondrocyte maturation through the network with SP7 and with FGF, Wnt, and IHH signaling pathways during skeletal Development. J. Cell. Biochem. 112: 750–755, 2011. © 2010 Wiley-Liss, Inc.
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Evaluation of 9.4-T MR microimaging in assessing normal and defective fetal Bone Development: comparison of MR imaging and histological findings
Bone, 2004Co-Authors: Yoko Ichikawa, Toshihisa Komori, Misa Sumi, Nobu Ohwatari, Tadateru Sumi, Hiroaki Shibata, Tatsuya Furuichi, Akira Yamaguchi, Takashi NakamuraAbstract:Abstract We evaluated 9.4-T magnetic resonance (MR) microimaging in assessing normal and defective Bone Development in mouse embryos. For this purpose, we performed 9.4-T MR microimaging on developing Bones in normal embryos, and also in Runx2/Cbfa1−/− embryos with severely defective Bone Development. MR images were compared with the histological and histochemical features of these fetal Bones. MR microimaging delineate successfully the normal long Bone Development in embryos. The T1- and T2-weighted MR microimaging demonstrated chondrocyte maturation in different regions of growing cartilage, such as epiphysis, physis, hypertrophic cartilage, and zone of provisional calcification. These Developmental changes were detectable in as early as E14.5 embryos. The MR microimaging clearly demonstrated defective Bone Development in Runx2/Cbfa1−/− embryos. The femur from E18.5 homozygous Runx2/Cbfa1−/− embryos lacked MR signal intensity patterns including the hypertrophic cartilage, which are characteristic of the Bone from the age-matched Runx2/Cbfa1+/+ embryos. Interestingly, however, the tibia from the same mutants was associated with MR signal patterns indicative of hypertrophic cartilage but not of the primary spongiosa and ossifying perichondrium, suggesting that Bone Development is differently regulated in these two long Bones. On the other hand, the Bones from heterozygous Runx2/Cbfa1+/− embryos exhibited an MR phenotype intermediate between the Runx2/Cbfa1+/+ and Runx2/Cbfa1−/− embryos; the primary spongiosa and ossifying perichondrium formation occurred normally even in the absence of preceding organized maturation of chondrocytes, a phenotype that was not detected by histological examinations. We concluded that MR microimaging is useful in assessing the Bone Development.
Eckhard Schoenau - One of the best experts on this subject based on the ideXlab platform.
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High and low birth weight and its implication for growth and Bone Development in childhood and adolescence.
Journal of Pediatric Endocrinology and Metabolism, 2009Co-Authors: Oliver Fricke, Oliver Semler, Angelika Stabrey, Baerbel Tutlewski, Thomas Remer, Peter Herkenrath, Eckhard SchoenauAbstract:AIM: To investigate the relationship of birth weight (BW) to anthropometric measures, local body composition and Bone Development. POPULATION AND METHODS: 284 individuals (age 5-19 yr, 145 females) were recruited from the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) study. Parameters of Bone Development (cortical Bone mineral density [BMDcort], endosteal circumference [CE]) and of local body composition (cross-sectional fat area [FA]) were analyzed by pQCT at the forearm. Parameters were transformed into SD scores to adjust for age or height. RESULTS: BW predicted weight-SDS (R = 0.221), height-SDS (R = 0.260) and FA-SDS (R = 0.150). Individuals with lower BW (< 10th percentile) had lower weight-SDS (p < 0.01), height-SDS (p < 0.01), BMDcort-SDS (p = 0.02) and higher CE-SDS (p = 0.05). BMDcort was correlated with BW (r = -0.319) and FA (r = -0.283) in pubertal females. CONCLUSION: BW is characterized by direct and indirect effects on growth, body composition and Bone Development.
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Fetal and postnatal Bone Development: reviewing the role of mechanical stimuli and nutrition.
Best Practice & Research Clinical Endocrinology & Metabolism, 2008Co-Authors: Christof Land, Eckhard SchoenauAbstract:Fetal and postnatal Bone Development is by tradition viewed as a process of Bone mineral accretion or an increase in Bone mass. Accordingly, previous approaches to Bone Development in neonatology and early childhood have emphasized the determinants of peak Bone mass and their relationship to osteopenia, osteoporosis and fractures in later life. This suggests that the neonatal period and early childhood is an important period for Bone mineral accrual, and that peak Bone mass may be correlated with subsequent skeletal health. Nevertheless, describing fetal and postnatal Bone Development just in terms of changes in mass or density means looking at Bones as if they were amorphous heaps of calcium and phosphorus. In reality, of course, Bones are complex three-dimensional structures. It is therefore important to create conditions that stimulate Bones to become more stable. We suggest that functional Bone physiology can be used to explain fetal and postnatal Bone Development and to devise strategies for improved Bone Development in both premature infants and neonates.
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Local body composition is associated with gender differences of Bone Development at the forearm in puberty.
Hormone Research, 2008Co-Authors: Oliver Fricke, Angelika Stabrey, Baerbel Tutlewski, Thomas Remer, Zdenek Sumnik, Eckhard SchoenauAbstract:Background/Aims: The present analyses intend to clarify if gender and puberty modify the relationship between Bone Development (modeling and remodeling) and fat mass at the forearm.
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The regulation of Bone Development as a biological system
HOMO, 2003Co-Authors: Eckhard Schoenau, Oliver Fricke, Frank RauchAbstract:Summary A large number of molecular, cellular, and epidemiologic factors have been implicated in the regulation of Bone Development. A major unsolved problem is how to integrate these disparate findings into a concept that explains the Development of Bone as an organ. Often, events at the organ level are simply presented as the cumulative effect of all factors that individually are known to influence Bone Development. In such a cumulative model it must be assumed that each Bone cell carries the construction plan of the entire skeletal anatomy in its genes. This scenario is implausible, because it would require an astronomical amount of positional information. We therefore propose a functional model of Bone Development, which is based on Frost's mechanostat theory. In this model, the genome only provides positional information for the basic outline of the skeleton as a cartilaginous template. Thereafter, Bone cell action is coordinated by the mechanical requirements of the Bone.