by Lee Kwong Man, Simon. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 239-277). / ABSTRACT --- p.i / ACKNOWLEDGMENT --- p.vi / PUBLICATIONS --- p.vii / ABBREVIATIONS --- p.viii / TABLE OF CONTENT --- p.xi / Chapter CHAPTER ONE --- General Introduction --- p.1 / Chapter CHAPTER TWO --- Identification and Biochemical Characterization of Various Differentiative Growth Plate Chondrocytes by Countercurrent Centrifugal Elutriation --- p.8 / Chapter CHAPTER THREE --- Differential Expression of Glycoconjugates during Endochondral Ossification in Porcine Growth Plate --- p.50 / Chapter CHAPTER FOUR --- Intra- & Extra-Cellular Free Calcium Activities of Porcine Growth Plate Chondrocytes at Various Stages of Maturation --- p.90 / Chapter CHAPTER FIVE --- A New In Situ Model for Electrophysiological Characterization of Ionic Channels in Growth Plate Chondrocytes --- p.144 / Chapter CHAPTER SIX --- Effects of Quinolones on Growth Plate Chondrocytes --- p.201 / Chapter CHAPTER SEVEN --- Summary and Conclusion --- p.226 / BIBLIOGRAPHY --- p.239

Thesis (Ph. D.)--Ohio State University, 1970. / Includes vita. Includes bibliographical references (leaves 67-77). Available online via OhioLINK's ETD Center.

Collagen production by skin fibroblast cell strains from normal subjects and age-matched patients with the mendelian disorder--Osteogenesis Imperfecta (OI)--was studied in culture. / Number of generations in culture, phase of growth, labelling times, and site of biopsy did not influence collagen production by normal skin fibroblasts. / OI cell strains from patients with dominantly inherited OI have abnormal morphology and growth in culture. The ratio of Type I to protype III collagen is reduced in OI Types I, II and IV (Sillence classification). Type III OI could not be distinguished from normal strains by the analysis used. From the collagen phenotype (biochemical parameters) we were able to distinguish different OI phenotypes and to correlate these with clinical phenotypes. One form of OI Type I produces an unstable collagen that is degraded to small peptides in culture.

Thesis (Ph.D.)--University of Missouri-Columbia, 2006. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on May 1, 2009) Vita. Includes bibliographical references.

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The differentiation of osteoblasts and bone marrow adipocytes are closely associated yet mutually exclusive processes that are essential for maintaining bone homeostasis. Various diseases have been shown to develop once the delicate balance between adipogenesis and osteoblastogenesis is disrupted. Investigating the underlying molecular mechanisms of the osteoblasto-adipogenic switch under osteoporotic conditions will facilitate our understanding of the pathogenesis of osteoporosis and may eventually lead to the development of clinical therapeutic approaches for this life-threatening disease. While changes in cell morphology and cytoskeletal integrity can alter pre-committed mesenchymal stem cell (MSC) differentiation of certain lineages, previous studies have shown that cellular morphological changes can affect the early commitment of pluripotent MSCs via modulation of Ras homolog gene family, member A (RhoA) activity. The RhoA pathway regulates actin polymerization to promote the incorporation of globular-actin (G-actin) into filamentous-actin (F-actin). Actin polymerization releases G-actin bound myocardin-related transcription factors (MRTFs), which translocate to the nucleus and co-activate serum response factor (SRF) target gene expression. Exactly how the RhoA-actin-MRTF-SRF circuit is involved in the regulation of early commitment of MSCs remains poorly understood. Here we show that global MRTFA knockout mice (MRTFA KO) exhibited lower body weight, shorter femur and tibia lengths, and decreased trabecular bone volume. Furthermore, bone marrow MSCs isolated from MRTFA KO mice showed increased adipogenesis and brown fat gene expression as well as compromised osteoblastogenic differentiation as compared to WT controls. Treatment of WT bone marrow MSCs with the SRF inhibitor, CCG1423, mimicked these effects in that the compound inhibited osteoblastogenesis and promoted adipogenesis. Over-expression of MRTFA or SRF inhibited adipogenesis and enhanced osteoblastogenesis in C3H/10T1/2 cell lines, whereas over-expression of dominant-negative MRTFA or SRF variants had the opposite effects. In conclusion, our study identified MRTFA as a crucial regulator of skeletal homeostasis via regulating the balance between adipogenic and osteoblastogenic differentiation of the MSCs. Furthering our understanding of how the RhoA-actin-MRTFA-SRF circuit is involved in regulating the fate commitment of MSCs may ultimately lead to novel therapeutic strategies for treating osteoporosis and obesity.

Thesis (Ph. D.)--University of Washington, 2001. / Vita. Includes bibliographical references (leaves 113-123).