An in vitro analysis of chondrogenesis utilizing the versican deficient hdf mutant mouse / by Dennis Ray Williams, Jr.

Author/creator Williams, Dennis Ray author.
Other author Capehart, Anthony A., degree supervisor.
Other author East Carolina University. Department of Biology.
Format Theses and dissertations
Production2004.
Description56 leaves : illustrations (some color) ; 28 cm
Supplemental ContentAccess via ScholarShip
Subjects

Summary Mesenchymal condensation or aggregation represents a pivotal process during endochondral skeletogenesis. Extracellular matrix (ECM) interactions have been previously reported to play a crucial role in the process of mesenchymal aggregation and subsequent cartilage differentiation. It has been suggested that the modular ECM proteoglycan, versican, plays a significant role in early events of skeletogenesis by virtue of its spatiotemporal expression pattern during mesenchymal aggregation and chondrogenesis. The versican-deficient hdf transgenic mouse has provided the first model to explore the implications of a null mature versican on chondrogenesis. Due to embryonic lethality of hdf homozygotes at 10.5 dpc, the well accepted high-density micromass culture system was employed to compare the in vitro chondrogenic capacity of hdf mutants to that of the wild type. Mesenchyme derived from hdf homozygous mutants demonstrated an inhibition of mesenchymal aggregation and an inability to produce cartilage characteristic molecules after 6 days of high-density micromass culture. Results of this study strongly suggest that versican is essential for mesenchymal aggregation and subsequent cartilage differentiation.
General notePresented to the faculty of the Department of Biology.
General noteAdvisor: Anthony A. Capehart
Dissertation noteM.S. East Carolina University 2004
Bibliography noteIncludes bibliographical references (leaves 39-46).
Genre/formAcademic theses.
Genre/formAcademic theses.
Genre/formThèses et écrits académiques.

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