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25 results on '"Cherman, Natasha"'

1. Lineage-specific differentiation of osteogenic progenitors from pluripotent stem cells reveals the FGF1-RUNX2 association in neural crest-derived osteoprogenitors.

Author

Kidwai, Fahad, Mui, Byron, Arora, Deepika, Iqbal, Kulsum, Hockaday, Madison, de Castro Diaz, Luis, Cherman, Natasha, Martin, Daniel, Myneni, Vamsee, Ahmad, Moaz, Futrega, Katarzyna, Ali, Sania, Merling, Randall, Lee, Janice, Robey, Pamela, and Kaufman, Dan

Subjects
bone development, cell differentiation, fibroblast growth factor 1, neural crest, osteogenesis, pluripotent stem cells, Animals, Cell Differentiation, Cell Lineage, Core Binding Factor Alpha 1 Subunit, Fibroblast Growth Factor 1, Humans, MAP Kinase Signaling System, Male, Mice, Neural Crest, Osteogenesis, Pluripotent Stem Cells, Principal Component Analysis, Transcriptome
Abstract

Human pluripotent stem cells (hPSCs) can provide a platform to model bone organogenesis and disease. To reflect the developmental process of the human skeleton, hPSC differentiation methods should include osteogenic progenitors (OPs) arising from three distinct embryonic lineages: the paraxial mesoderm, lateral plate mesoderm, and neural crest. Although OP differentiation protocols have been developed, the lineage from which they are derived, as well as characterization of their genetic and molecular differences, has not been well reported. Therefore, to generate lineage-specific OPs from human embryonic stem cells and human induced pluripotent stem cells, we employed stepwise differentiation of paraxial mesoderm-like cells, lateral plate mesoderm-like cells, and neural crest-like cells toward their respective OP subpopulation. Successful differentiation, confirmed through gene expression and in vivo assays, permitted the identification of transcriptomic signatures of all three cell populations. We also report, for the first time, high FGF1 levels in neural crest-derived OPs-a notable finding given the critical role of fibroblast growth factors (FGFs) in osteogenesis and mineral homeostasis. Our results indicate that FGF1 influences RUNX2 levels, with concomitant changes in ERK1/2 signaling. Overall, our study further validates hPSCs power to model bone development and disease and reveals new, potentially important pathways influencing these processes.

Published
2020

14. Lineage‐specific differentiation of osteogenic progenitors from pluripotent stem cells reveals the FGF1‐RUNX2association in neural crest‐derived osteoprogenitors

Author

Kidwai, Fahad, Mui, Byron W. H., Arora, Deepika, Iqbal, Kulsum, Hockaday, Madison, Castro Diaz, Luis Fernandez, Cherman, Natasha, Martin, Daniel, Myneni, Vamsee D., Ahmad, Moaz, Futrega, Katarzyna, Ali, Sania, Merling, Randall K., Kaufman, Dan S., Lee, Janice, and Robey, Pamela G.

Abstract

Human pluripotent stem cells (hPSCs) can provide a platform to model bone organogenesis and disease. To reflect the developmental process of the human skeleton, hPSC differentiation methods should include osteogenic progenitors (OPs) arising from three distinct embryonic lineages: the paraxial mesoderm, lateral plate mesoderm, and neural crest. Although OP differentiation protocols have been developed, the lineage from which they are derived, as well as characterization of their genetic and molecular differences, has not been well reported. Therefore, to generate lineage‐specific OPs from human embryonic stem cells and human induced pluripotent stem cells, we employed stepwise differentiation of paraxial mesoderm‐like cells, lateral plate mesoderm‐like cells, and neural crest‐like cells toward their respective OP subpopulation. Successful differentiation, confirmed through gene expression and in vivo assays, permitted the identification of transcriptomic signatures of all three cell populations. We also report, for the first time, high FGF1 levels in neural crest‐derived OPs—a notable finding given the critical role of fibroblast growth factors (FGFs) in osteogenesis and mineral homeostasis. Our results indicate that FGF1 influences RUNX2 levels, with concomitant changes in ERK1/2 signaling. Overall, our study further validates hPSCs' power to model bone development and disease and reveals new, potentially important pathways influencing these processes. Human pluripotent stem cells were stepwise differentiated toward paraxial mesoderm‐, lateral plate mesoderm‐, and neural crest‐derived osteogenic progenitors (OPs). Transcriptomic signatures of these three cell subpopulations were identified, with a new finding of high FGF1 levels and its association with RUNX2 in neural crest‐derived OPs.

Published
2020
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16. Directed Differentiation of Human Induced Pluripotent Stem Cells Toward Bone and Cartilage: In Vitro Versus In Vivo Assays

Author

Phillips, Matthew D., primary, Kuznetsov, Sergei A., additional, Cherman, Natasha, additional, Park, Kyeyoon, additional, Chen, Kevin G., additional, McClendon, Britney N., additional, Hamilton, Rebecca S., additional, McKay, Ronald D.G., additional, Chenoweth, Josh G., additional, Mallon, Barbara S., additional, and Robey, Pamela G., additional

Published
2014
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17. GNAS transcripts in skeletal progenitors:evidence for random asymmetric allelic expression of Gs alpha

Author

Michienzi, Stefano, Cherman, Natasha, Holmbeck, Kenn, Funari, Alessia, Collins, Michael T, Bianco, Paolo, Robey, Pamela Gehron, Riminucci, Mara, Michienzi, Stefano, Cherman, Natasha, Holmbeck, Kenn, Funari, Alessia, Collins, Michael T, Bianco, Paolo, Robey, Pamela Gehron, and Riminucci, Mara

Abstract

Activating mutations of the Gsalpha gene, encoded by the guanine nucleotide-binding protein, alpha stimulating (GNAS) locus located on chromosome 20q13, underlie different clinical phenotypes characterized by skeletal lesions [fibrous dysplasia (FD) of bone], extraskeletal diseases (mainly endocrine hyperfunction and skin hyperpigmentation) and variable combinations thereof [the McCune-Albright syndrome (MAS)]. This clinical heterogeneity is commonly assumed to reflect the post-zygotic origin of the mutation. However, the pattern of imprinting of the Gsalpha gene in some human post-natal tissues suggests that parental-dependent epigenetic mechanisms may also play a role in the phenotypic effect of the mutated GNAS genotype. FD lesions are generated by mutated clonogenic osteoprogenitors that reside, along with their normal counterparts, in FD bone marrow stroma. We analyzed the allelic expression pattern of Gsalpha and other GNAS alternative transcripts in the progeny of normal and mutated clonogenic stromal cells isolated in vitro from a series of informative FD/MAS patients. We report here for the first time that the two Gsalpha alleles are unequally expressed in both normal and FD-mutated stromal clones. However, in contrast to imprinting, the ratio of Gsalpha allelic expression is randomly established in different clones from the same patient. This result suggests that a parental-independent modulation of Gsalpha expression occurs in clonogenic osteoprogenitor cells and, at the single cell level, may impact on the severity of an FD lesion. Furthermore, we show that normal and mutated clonogenic stromal cells express GNAS alternative transcripts other than the common Gsalpha, some of which may be relevant to the development of FD.

Published
2007

18. Denosumab treatment for fibrous dysplasia

Author

Boyce, Alison M, primary, Chong, William H, additional, Yao, Jack, additional, Gafni, Rachel I, additional, Kelly, Marilyn H, additional, Chamberlain, Christine E, additional, Bassim, Carol, additional, Cherman, Natasha, additional, Ellsworth, Michelle, additional, Kasa‐Vubu, Josephine Z, additional, Farley, Frances A, additional, Molinolo, Alfredo A, additional, Bhattacharyya, Nisan, additional, and Collins, Michael T, additional

Published
2012
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19. Mechanism of FGF23 processing in fibrous dysplasia

Author

Bhattacharyya, Nisan, primary, Wiench, Malgorzata, additional, Dumitrescu, Claudia, additional, Connolly, Brian M, additional, Bugge, Thomas H, additional, Patel, Himatkumar V, additional, Gafni, Rachel I, additional, Cherman, Natasha, additional, Cho, Monique, additional, Hager, Gordon L, additional, and Collins, Michael T, additional

Published
2012
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24. Age-Dependent Demise of GNAS-Mutated Skeletal Stem Cells and "Normalization" of Fibrous Dysplasia of Bone.

Author

Kuznetsov, Sergei A., Cherman, Natasha, Riminucci, Mara, Collins, Michael T., Robey, Pamela Gehron, and Bianco, Paolo

Abstract

The article reports on the results of research which was conducted in an effort to determine the role that somatic mosaicism in fibrous dysplasia of bone within the context of skeletal (mesenchymal) stem cells play. Researchers assessed the frequency of mutated colony forming unit-fibroblasts from lesions and other sites in patients. They found that as lesions age, mutant stem cells survive, self renew and enable formation of a normal structure and that GNAS mutations disrupt cell renewal.

Published
2008
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25. Monostotic Fibrous Dysplasia of the Proximal Femur and Liposclerosing Myxofibrous Tumor: Which One Is Which?

Author

Corsi, Alessandro, De Maio, Fernando, Ippolito, Ernesto, Cherman, Natasha, Robey, Pamela Gehron, Riminucci, Mara, and Bianco, Paolo

Abstract

The article presents the clinical, histological, and genetic studies of two cases of isolated fibro-osseous lesions of the femur in adults. It shows the overlap between monostotic fibrous dysplasia (MFD) of the proximal femur and the liposclerosin myxofibrous tumor. The two cases highlight how the incomplete understanding of the natural history of MFD may result in diagnostic pitfalls or incorrect classification of individual lesions.

Published
2006
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