Готові списки джерел за темами / Murine skeletal development

Добірка наукової літератури з теми "Murine skeletal development"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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Статті в журналах з теми "Murine skeletal development"

Marchini, Marta, Elizabeth Silva Hernandez, and Campbell Rolian. "Morphology and development of a novel murine skeletal dysplasia." PeerJ 7 (July 4, 2019): e7180. http://dx.doi.org/10.7717/peerj.7180.

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Background Limb bones develop and grow by endochondral ossification, which is regulated by specific cell and molecular pathways. Changes in one or more of these pathways can have severe effects on normal skeletal development, leading to skeletal dysplasias. Many skeletal dysplasias are known to result from mis-expression of major genes involved in skeletal development, but the etiology of many skeletal dysplasias remains unknown. We investigated the morphology and development of a mouse line with an uncharacterized mutation exhibiting a skeletal dysplasia-like phenotype (Nabo). Methods We used µCT scanning and histology to comprehensively characterize the phenotype and its development, and to determine the developmental stage when this phenotype first appears. Results Nabo mice have shorter limb elements compared to wildtype mice, while clavicles and dermal bones of the skull are not affected. Nabo embryos at embryonic stage E14 show shorter limb cartilage condensations. The tibial growth plate in Nabo mice is wider than in wildtype, particularly in the proliferative zone, however proliferative chondrocytes show less activity than wildtype mice. Cell proliferation assays and immunohistochemistry against the chondrogenic marker Sox9 suggest relatively lower, spatially-restricted, chondrocyte proliferation activity in Nabo. Bone volume and trabecular thickness in Nabo tibiae are also decreased compared to wildtype. Discussion Our data suggest that the Nabo mutation affects endochondral ossification only, with the strongest effects manifesting in more proximal limb structures. The phenotype appears before embryonic stage E14, suggesting that outgrowth and patterning processes may be affected. Nabo mice present a combination of skeletal dysplasia-like characteristics not present in any known skeletal dysplasia. Further genomic and molecular analysis will help to identify the genetic basis and precise developmental pathways involved in this unique skeletal dysplasia.

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Xie, Meng, Dmitrii Kamenev, Marketa Kaucka, Maria Eleni Kastriti, Baoyi Zhou, Artem V. Artemov, Mekayla Storer, et al. "Schwann cell precursors contribute to skeletal formation during embryonic development in mice and zebrafish." Proceedings of the National Academy of Sciences 116, no. 30 (July 8, 2019): 15068–73. http://dx.doi.org/10.1073/pnas.1900038116.

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Immature multipotent embryonic peripheral glial cells, the Schwann cell precursors (SCPs), differentiate into melanocytes, parasympathetic neurons, chromaffin cells, and dental mesenchymal populations. Here, genetic lineage tracing revealed that, during murine embryonic development, some SCPs detach from nerve fibers to become mesenchymal cells, which differentiate further into chondrocytes and mature osteocytes. This occurred only during embryonic development, producing numerous craniofacial and trunk skeletal elements, without contributing to development of the appendicular skeleton. Formation of chondrocytes from SCPs also occurred in zebrafish, indicating evolutionary conservation. Our findings reveal multipotency of SCPs, providing a developmental link between the nervous system and skeleton.

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Magnani, D. M., E. T. Lyons, T. S. Forde, M. T. Shekhani, V. A. Adarichev, and G. A. Splitter. "Osteoarticular tissue infection and development of skeletal pathology in murine brucellosis." Disease Models & Mechanisms 6, no. 3 (March 8, 2013): 811–18. http://dx.doi.org/10.1242/dmm.011056.

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Yokota, Masaya, Kotaro Suzuki, Daiki Nakagomi, Koji Tokoyoda, Toshinori Nakayama, Hitoshi Kohsaka, Itsuo Iwamoto, and Hiroshi Nakajima. "Crucial roles of mast cells in the development of a murine model of polymyositis (171.20)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 171.20. http://dx.doi.org/10.4049/jimmunol.188.supp.171.20.

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Abstract Objective: In addition to a pivotal role of mast cells in allergic diseases, recent data suggest that mast cells play a crucial role in a variety of immune responses. However, their role in the pathogenesis of autoimmune skeletal muscle diseases has not been clarified despite their distribution in skeletal muscle. Therefore, the objective of this study is to determine the role of mast cells in the development of a murine model of polymyositis, C protein-induced myositis (CIM). Methods: The susceptibility of mast cell-deficient WBB6F1-KitW/KitWv mice (W/Wv mice) to CIM was compared with that of wild-type (WT) mice. The effect of mast cell reconstitution with bone marrow-derived mast cells (BMMCs) on the susceptibility of W/Wv mice to CIM was also evaluated. Results: W/Wv mice exhibited significantly reduced disease incidence and histological scores of CIM as compared with WT mice. The infiltration of macrophages but not of CD8+ T cells in the skeletal muscle was attenuated in CIM of W/Wv mice. The expression of monocyte chemotactic protein-1 (MCP-1) in skeletal muscle was reduced in W/Wv mice. Vascular permeability in skeletal muscle was elevated in WT mice but not in W/Wv mice upon CIM induction. Engraftment of BMMCs restored the incidence and histological scores of CIM in W/Wv mice. Conclusion: Mast cells play critical roles in the development of CIM.

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Sotiriou, V., Y. Huang, S. Ahmed, H. Isaksson, and NC Nowlan. "Prenatal murine skeletogenesis partially recovers from absent skeletal muscle as development progresses." European Cells and Materials 44 (November 8, 2022): 115–32. http://dx.doi.org/10.22203/ecm.v044a08.

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Skeletal muscle contractions are critical for normal skeletal growth and morphogenesis but it is unclear how the detrimental effects of absent muscle on the bones and joints change over time. Joint shape and cavitation as well as rudiment length and mineralisation were assessed in multiple rudiments at two developmental stages [Theiler stage (TS)24 and TS27] in the splotch-delayed “muscle-less limb” mouse model and littermate controls. Chondrocyte morphology was quantified in 3D in the distal humerus at the same stages. As development progressed, the effects of absent muscle on all parameters except for cavitation become less severe. All major joints in muscle-less limbs were abnormally shaped at TS24, while, by TS27, most muscle-less limb joint shapes were normal or nearly normal. In contrast, any joints that were fused at TS24 did not cavitate by TS27. At TS24, chondrocytes in the distal humerus were significantly smaller in the muscle-less limbs than in controls, while by TS27, chondrocyte volume was similar between the two groups, offering a cell-level mechanism for the partial recovery in shape of muscle-less limbs. Mineralisation showed the most pronounced changes over gestation. At TS24, all muscle-less rudiments studied had less mineralisation than the controls, while at TS27, muscle-less limb rudiments had mineralisation extents equivalent to controls. In conclusion, the effects of muscle absence on prenatal murine skeletogenesis reduced in severity over gestation. Understanding how mammalian bones and joints continue to develop in an environment with abnormal fetal movements provides insights into conditions including hip dysplasia and arthrogryposis.

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Khavandgar, Zohreh, Christophe Poirier, Christopher J. Clarke, Jingjing Li, Nicholas Wang, Marc D. McKee, Yusuf A. Hannun, and Monzur Murshed. "A cell-autonomous requirement for neutral sphingomyelinase 2 in bone mineralization." Journal of Cell Biology 194, no. 2 (July 25, 2011): 277–89. http://dx.doi.org/10.1083/jcb.201102051.

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A deletion mutation called fro (fragilitas ossium) in the murine Smpd3 (sphingomyelin phosphodiesterase 3) gene leads to a severe skeletal dysplasia. Smpd3 encodes a neutral sphingomyelinase (nSMase2), which cleaves sphingomyelin to generate bioactive lipid metabolites. We examined endochondral ossification in embryonic day 15.5 fro/fro mouse embryos and observed impaired apoptosis of hypertrophic chondrocytes and severely undermineralized cortical bones in the developing skeleton. In a recent study, it was suggested that nSMase2 activity in the brain regulates skeletal development through endocrine factors. However, we detected Smpd3 expression in both embryonic and postnatal skeletal tissues in wild-type mice. To investigate whether nSMase2 plays a cell-autonomous role in these tissues, we examined the in vitro mineralization properties of fro/fro osteoblast cultures. fro/fro cultures mineralized less than the control osteoblast cultures. We next generated fro/fro;Col1a1-Smpd3 mice, in which osteoblast-specific expression of Smpd3 corrected the bone abnormalities observed in fro/fro embryos without affecting the cartilage phenotype. Our data suggest tissue-specific roles for nSMase2 in skeletal tissues.

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Vanyai, Hannah K., Fabrice Prin, Oriane Guillermin, Bishara Marzook, Stefan Boeing, Alexander Howson, Rebecca E. Saunders, et al. "Control of skeletal morphogenesis by the Hippo-YAP/TAZ pathway." Development 147, no. 21 (September 29, 2020): dev187187. http://dx.doi.org/10.1242/dev.187187.

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ABSTRACTThe Hippo-YAP/TAZ pathway is an important regulator of tissue growth, but can also control cell fate or tissue morphogenesis. Here, we investigate the function of the Hippo pathway during the development of cartilage, which forms the majority of the skeleton. Previously, YAP was proposed to inhibit skeletal size by repressing chondrocyte proliferation and differentiation. We find that, in vitro, Yap/Taz double knockout impairs murine chondrocyte proliferation, whereas constitutively nuclear nls-YAP5SA accelerates proliferation, in line with the canonical role of this pathway in most tissues. However, in vivo, cartilage-specific knockout of Yap/Taz does not prevent chondrocyte proliferation, differentiation or skeletal growth, but rather results in various skeletal deformities including cleft palate. Cartilage-specific expression of nls-YAP5SA or knockout of Lats1/2 do not increase cartilage growth, but instead lead to catastrophic malformations resembling chondrodysplasia or achondrogenesis. Physiological YAP target genes in cartilage include Ctgf, Cyr61 and several matrix remodelling enzymes. Thus, YAP/TAZ activity controls chondrocyte proliferation in vitro, possibly reflecting a regenerative response, but is dispensable for chondrocyte proliferation in vivo, and instead functions to control cartilage morphogenesis via regulation of the extracellular matrix.

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Tribioli, C., and T. Lufkin. "The murine Bapx1 homeobox gene plays a critical role in embryonic development of the axial skeleton and spleen." Development 126, no. 24 (December 15, 1999): 5699–711. http://dx.doi.org/10.1242/dev.126.24.5699.

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Our previous studies in both mouse and human identified the Bapx1 homeobox gene, a member of the NK gene family, as one of the earliest markers for prechondrogenic cells that will subsequently undergo mesenchymal condensation, cartilage production and, finally, endochondral bone formation. In addition, Bapx1 is an early developmental marker for splanchnic mesoderm, consistent with a role in visceral mesoderm specification, a function performed by its homologue bagpipe, in Drosophila. The human homologue of Bapx1 has been identified and mapped to 4p16.1, a region containing loci for several skeletal diseases. Bapx1 null mice are affected by a perinatal lethal skeletal dysplasia and asplenia, with severe malformation or absence of specific bones of the vertebral column and cranial bones of mesodermal origin, with the most severely affected skeletal elements corresponding to ventral structures associated with the notochord. We provide evidence that the failure of the formation of skeletal elements in Bapx1 null embryos is a consequence of a failure of cartilage development, as demonstrated by downregulation of several molecular markers required for normal chondroblast differentiation (α 1(II) collagen, Fgfr3, Osf2, Indian hedgehog, Sox9), as well as a chondrocyte-specific alpha1 (II) collagen-lacZ transgene. The cartilage defects are correlated with failed differentiation of the sclerotome at the time when these cells are normally initiating chondrogenesis. Loss of Bapx1 is accompanied by an increase in apoptotic cell death in affected tissues, although cell cycling rates are unaltered.

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Iqbal, Aqsa, Ulrike May, Stuart N. Prince, Tero A. H. Järvinen та Ahlke Heydemann. "Systemically Administered Homing Peptide Targets Dystrophic Lesions and Delivers Transforming Growth Factor-β (TGFβ) Inhibitor to Attenuate Murine Muscular Dystrophy Pathology". Pharmaceutics 13, № 9 (18 вересня 2021): 1506. http://dx.doi.org/10.3390/pharmaceutics13091506.

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Muscular dystrophy is a progressively worsening and lethal disease, where accumulation of functionality-impairing fibrosis plays a key pathogenic role. Transforming growth factor-β1 (TGFβ1) is a central signaling molecule in the development of fibrosis in muscular dystrophic humans and mice. Inhibition of TGFβ1 has proven beneficial in mouse models of muscular dystrophy, but the global strategies of TGFβ1 inhibition produce significant detrimental side effects. Here, we investigated whether murine muscular dystrophy lesion-specific inhibition of TGFβ1 signaling by the targeted delivery of therapeutic decorin (a natural TGFβ inhibitor) by a vascular homing peptide CAR (CARSKNKDC) would reduce skeletal muscle fibrosis and pathology and increase functional characteristics of skeletal muscle. We demonstrate that CAR peptide homes to dystrophic lesions with specificity in two muscular dystrophy models. Recombinant fusion protein consisting of CAR peptide and decorin homes selectively to sites of skeletal muscle damage in mdxDBA2/J and gamma-sarcoglycan deficient DBA2/J mice. This targeted delivery reduced TGFβ1 signaling as demonstrated by reduced nuclear pSMAD staining. Three weeks of targeted decorin treatment decreased both membrane permeability and fibrosis and improved skeletal muscle function in comparison to control treatments in the mdxD2 mice. These results show that selective delivery of decorin to the sites of skeletal muscle damage attenuates the progression of murine muscular dystrophy.

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Abe, Makoto, Naoya Saeki, Yuki Ikeda, and Shinsuke Ohba. "Kruppel-like Factors in Skeletal Physiology and Pathologies." International Journal of Molecular Sciences 23, no. 23 (December 2, 2022): 15174. http://dx.doi.org/10.3390/ijms232315174.

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Kruppel-like factors (KLFs) belong to a large group of zinc finger-containing transcription factors with amino acid sequences resembling the Drosophila gap gene Krüppel. Since the first report of molecular cloning of the KLF family gene, the number of KLFs has increased rapidly. Currently, 17 murine and human KLFs are known to play crucial roles in the regulation of transcription, cell proliferation, cellular differentiation, stem cell maintenance, and tissue and organ pathogenesis. Recent evidence has shown that many KLF family molecules affect skeletal cells and regulate their differentiation and function. This review summarizes the current understanding of the unique roles of each KLF in skeletal cells during normal development and skeletal pathologies.

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Більше джерел

Дисертації з теми "Murine skeletal development"

Hemming, Sarah Elizabeth. "Epigenetic regulation of histone three lysine twenty seven tri methylation dictates mesenchymal stem cell lineage commitment, lifespan and murine skeletal development." Thesis, 2016. http://hdl.handle.net/2440/104715.

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Epigenetic modifiers are increasingly being implicated as playing major roles in many cellular and biological processes, such as cell growth, differentiation, lifespan, selfrenewal, cancer, and metastasis. Epigenetic modifying proteins such as Enhancer of Zeste homology 2 (EZH2), Lysine demethylase 6A (KDM6A) regulates chromatin structure through the addition or removal histone three lysine twenty seven (H3K27) tri methylation (me3) modification. The presence of H3K27me3 on the promoter of genes leads to the recruitment of chromatin condensation complexes, chromatin compaction and repression of genes transcription. H3K27 demethylases remove the H3K27me3 modification allowing the recruitment of activating transcriptional complexes, opening up of chromatin and gene expression. The Project is based on our initial profiling of histone methylation patterns of genes associated with differentiation and the expression of epigenetic modifying enzymes in MSC clonal populations by cDNA microarray analysis. Our initial studies on the function of EZH2 lineage commitment of human BMSC, suggests that EZH2 is a negative regulator of osteogenesis and a positive regulator of adipogenesis. However, the direct role of the H3K7me3 epigenetic modifiers EZH2 and KDM6A and or KDM6B in BMSC differentiation is unclear, illustrating the importance of determining the epigenetic signatures associated with differentiation and maintenance of MSC. Additionally, EZH2 mutations in one allele of EZH2 methyltransferase SET domain have been identified in patents with Weaver Syndrome. These patients exhibit excess bone growth, aging and mental retardation suggesting the importance of EZH2 in human bone development. Furthermore, with the current use of MSC for Phase II/III clinical trials it’s important to understanding of the molecular pathways and epigenetic changes that regulate maintenance and differentiation of MSC aiding in treatment of skeletal tissue disorders/diseases. Therefore this PhD project identifies that EZH2 and KDM6A acts as a switch regulating MSC lineage commitment. Presence of EZH2 and its H3K27me3 on osteogenic genes such as RUNX2 prevent MSC osteogenic differentiation and intern allows the progression of adipogenic differentiation of MSC. During osteogenesis we believe KDM6A play a role in removing the H3K27me3 off genes critical for osteogenic differentiation. Furthermore during osteogenic differentiation, EZH2 and its H3K27 modifications must be removed from genes such as RUNX2, ZBTB16, MX1 and FHL1 allowing the activation of these genes which are important for osteogenic differentiation. EZH2 conditional deletion in early limb bud mesenchyme reveals EZH2 plays a critical role in skeletal patterning, bone microarchitecture and remodelling.
Thesis (Ph.D.) (Research by Publication) -- University of Adelaide, School of Medicine, 2016.

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Pennimpede, Tracie. "CYP26B1 limits inappropriate activation of RARgamma by retinoic acid during murine embryogenesis." Thesis, 2010. http://hdl.handle.net/1974/7633.

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Proper embryonic patterning requires precise spatio-temporal regulation of retinoic acid (RA) activity. Morphogenesis can be regulated at the level of RA distribution, mainly via its synthesis and catabolism by the RALDH and CYP26 enzymes respectively, and at the level of RA-mediated transcription through activation of its cognate nuclear receptor, the retinoic acid receptors (RARs) α, β, and γ. Loss of Cyp26b1 leads to increased local levels of RA in tissues such as the limb and craniofacial structures, and results in neonatal lethality. Visible gross phenotypic defects in neonates include phocomelia (shortening of the limbs), adactyly (missing digits), micrognathia (shortened lower jaw), and open eyes at birth. In addition, these embryos exhibit cleft palate and have a paucity of vibrissal (whisker) and pelage (hair) follicles. We have previously shown that ablating the gene encoding RARγ in a Cyp26a1-null background was able to rescue the caudal abnormalities associated with improper RA exposure in these embryos by limiting aberrant RA signalling, and thus rescuing expression domains of target genes involved in caudal development. I show here that ablating Rarg in a Cyp26b1-null background is able to partially rescue the defects associated with loss of CYP26B1. These include a reduction in the severity of limb defects, rescued vibrissae, fused eyelids, and recovered aspects of axial skeletal development. This compound-null murine model illustrates that RARγ plays a specific role in transducing the RA signal within tissues that are affected by the loss of CYP26B1. Further molecular analysis of the pathways responsible for directing limb bud outgrowth and eyelid fusion provided insight into pathways regulated by RARγ in these rescued tissues.
Thesis (Ph.D, Pathology & Molecular Medicine) -- Queen's University, 2010-04-01 15:38:52.05

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Частини книг з теми "Murine skeletal development"

Grattan, M. J., C. Kondo, J. Thurston, P. Alakija, B. J. Burke, C. Stewart, D. Syme, and W. R. Giles. "Skeletal and Cardiac Muscle Defects in a Murine Model of Emery-Dreifuss Muscular Dystrophy." In Nuclear Organization in Development and Disease, 118–39. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470093765.ch9.

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Downey, Charlene M., and Frank R. Jirik. "Selenoproteins in Skeletal Development and Disease: Lessons from Trsp Deletion in Murine Bone and Cartilage Progenitor Cells." In Selenium, 573–87. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-1025-6_45.

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Тези доповідей конференцій з теми "Murine skeletal development"

Gefen, Amit, Bastiaan van Nierop, Dan L. Bader, and Cees W. Oomens. "A Method for Determining the Strain-Time Endurance of Cells in Planar Tissue-Engineered Constructs Subjected to Large Compressive Deformations." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192322.

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The mechanical environment of cells influences their normal growth and function, and may also affect the development of diseases and chronic injuries. Accordingly, there is substantial interest in determining the endurance of cells subjected to controlled mechanical strains for given time periods. A standardized, generic experimental method for determining strain-time thresholds for cell death is so far missing in the literature. In this study, a new experimental method was developed to measure strain-time thresholds of cells in planar tissue-engineered constructs subjected to large compressive strains. The method was applied to measure a strain-time threshold for differentiated C2C12 murine skeletal muscle cells in tissue-engineered bio-artificial muscle (BAM) constructs.

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Nasr, Saghar, and Neil A. Duncan. "Simulation of Tissue Differentiation During Fracture Healing Within a Collagenous Scaffold Implanted in a Murine Tibia With an Oblique Fracture." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80852.

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It is known that mechanical factors play a key role in bone formation and regulation of tissue regeneration during skeletal healing. However, the underlying mechanisms are not fully understood. Mechanical loads, such as cyclic compression, torsion and bending are key factors driving the differentiation of mesenchymal stem cells (MSCs). On the other hand, excessive mechanical loading may disrupt the process of healing and lead to non-unions and cell apoptosis. Therefore, effective positive mechanical factors are bounded by a range and frequency. A number of mechanoregulation algorithms have been developed by comparing tissue differentiation patterns under different loading regimes [1, 2, 3, 4]. The aim of this study was to predict the development of differentiated tissues in a closed fracture model treated with a stem cell seeded soft collagenous scaffold under load regimes of axial compression, bending and torsion. The long term goal is to improve our understanding of fracture healing in non-union fractures and develop stem cell based tissue engineering treatments.

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Papoutsakis, Konstantinos, Manolis Lourakis, and Maria Pateraki. "Automatic assessment of posture deviations in assembly tasks." In 13th International Conference on Applied Human Factors and Ergonomics (AHFE 2022). AHFE International, 2022. http://dx.doi.org/10.54941/ahfe1002145.

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The aim of this study is to investigate the development and the evaluation of a computer vision-based framework to aid the automatic assessment of posture deviations in assembly tasks in realistic work environments. A posture deviation refers to a time-varying working posture performed by the worker, that deviates from ergonomically safe body postures expected in the context of particular work tasks and is known to impose increased physical strain. The estimation of their occurrences can serve as indicators, known as risk factors, for the assessment of physical ergonomics towards the prevention of physical strain and in the-long-term of work-related musculo-skeletal disorders (WMSD). Using visual information acquired by camera sensors, our goal is to estimate the full body motion of a line worker in 3D space, unobtrusively, and to perform classification of four types of posture deviations, also noted as ergonomically sub-optimal working postures that were employed by the MURI risk analysis tool. We formulate a learning-based action classification task using Deep Graph-based Neural Networks and differential temporal alignment cost as a classification measure to estimate the type and risk level of the observed posture deviation during work activities. To evaluate the efficiency of the proposed approach, a new video dataset was captured in the context of the sustAGE project, that demonstrate two different workers during car door assembly actions in a simulated production line in an actual workplace. Rich annotation data were provided by experts in manufacturing and ergonomics. Both quantitative and qualitative evaluation of the proposed framework provide evidence for its efficiency and reliability in supporting ergonomic risk assessment and preventive actions for WMSD in real working environments.

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