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Regulation of cellular senescence in human fibroblasts /Benanti, Jennifer Ann. January 2003 (has links)
Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 106-118).
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POSSIBLE ROLE OF FIBRONECTIN IN THE PATHOGENESIS OF DUCHENNE'S MUSCULAR DYSTROPHY.ULREICH, JUDITH BABB. January 1987 (has links)
Fibronectin (FN) is a critical component of the extracellular matrix (ECM) of fibroblasts and muscle cells and contributes to the maintenance of cell cytoskeleton, shape, migration, growth and differentiation. Extensive accumulation of both collagen and FN occurs in skeletal muscle of patients with Duchenne's muscular dystrophy (DMD). Several researchers have recently claimed that FN can interfere with proper muscle differentiation. Our hypothesis is that DMD fibroblasts or muscle cells fail to regulate properly the type, synthesis, or secretion of FN and that the increased accumulation FN in the ECM of fibroblasts in muscle may interfere with myogenesis, thus presenting the typical picture of regenerating but largely non-functional muscle in DMD. This was tested by labeling cultures of fibroblasts from DMD patients and controls with ³⁵S-methionine and quantitating basal levels of FN synthesis and degradation by immunoprecipitation. Collagen, FN and other components were measured in DMD sera and the metabolic effects of culturing DMD and control fibroblasts in the presence of DMD sera were studied. Muscle biopsies from DMD patients were examined for factors which might contribute to the accumulation of connective tissue. Increased levels of FN were measured in sera and cultured fibroblasts from DMD patients. Concomitant increases in other ECM components (collagen, glycosaminoglycans) were measured. The FN accumulation is at the expense of other cellular proteins as RNA and protein synthesis are reduced in DMD fibroblasts. Protein degradation studies indicate that reduced catabolism of FN may account for significant elevations in cells and sera. DMD sera cultured on control fibroblasts caused metabolic alterations reminiscent of dystrophic cells (increased FN and collagen accumulation, decreased RNA synthesis). Many of the observed metabolic changes are age-related in DMD, increasing in older patients. These results suggest that overproduction by fibroblasts and increased serum levels of components of the ECM in DMD may influence the accumulation of connective tissue in DMD muscle. DMD may not be of myopathic origin but an increased compartment of fibroblasts and macrophages as observed in DMD muscle may result from chemotactic mobilization caused by elevated FN and/or collagen in the tissue.
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Role of interleukin-15 and nitric oxide expression in chronic inflammatory diseaseLeung, Bernard P. January 1998 (has links)
No description available.
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Regulation of prostaglandin E₂ synthesis in human gingival fibroblasts /Yucel-Lindberg, Tülay, January 1900 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.
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Metabolism and macromolecular binding of benzo(a)pyrene by transformable and non-transformable human skin fibroblast cells /Tejwani, Raman Chitkara January 1980 (has links)
No description available.
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Functional characterization of cancer-associated fibroblasts in the regulation of cancer stem cell-like properties in hepatocellular carcinomaLau, Yuen-ting, 劉婉婷 January 2015 (has links)
abstract / Pathology / Doctoral / Doctor of Philosophy
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Effect of zinc supplementation on cell growth and lipoprotein binding in human fibroblast cellsShimakawa, Tomoko 27 April 1983 (has links)
Normal human skin fibroblast cells were used to study the effect
of zinc supplementation of the media on cell growth and the competitive
binding activity of low density lipoprotein (LDL). Cells were
grown in the media containing Dulbecco's Modified-Eagle Medium (DMEM),
5% (v/v) fetal calf serum (FCS), and various levels of zinc. Cell
counts and protein determination revealed that there was no stimulatory
effect of zinc on the growth of cells, showing a flat growth
curve with up to 6 μg/ml zinc supplementation. However, zinc supplementation
of greater than 6 μg/ml to the medium appeared to be toxic
to the cell and thereby prevented growth. When zinc was removed from
the medium using Epoxy-activated Sepharose 6B coupled with iminodiacetate,
zinc concentration in the medium was markedly reduced to 0.045
μg/ml from 0.210 μg/ml. The cell growth study using this zinc depleted
medium exhibited a growth curve similar to that obtained from
the earlier study, suggesting that 0.045 μg/ml of zinc in the control
medium was still sufficient to support normal cell growth. For the
LDL binding study, cells were grown in the media with various levels
of zinc supplementation for 7 days and the competitive binding activity
of LDL was determined. When cells were grown in the zinc removed
medium with 1.5 μg/ml zinc supplementation, the maximum amounts
of ¹²⁵I-LDL bound and internalized in the cells were observed; however,
higher levels of zinc supplementation to the growth medium caused decreased ¹²⁵I-LDL binding to the cell receptors. These
results suggest that zinc may be involved in the binding of LDL to
the receptors. / Graduation date: 1983
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HEAT SHOCK PROTEIN SYNTHESIS AND THERMOTOLERANCE EXPRESSION IN RAT EMBRYONIC FIBROBLASTS (HYPERTHERMIA, GENE REGULATION).WIDELITZ, RANDALL BRUCE. January 1986 (has links)
In response to a variety of hyperthermic treatments, rat embryonic fibroblasts synthesize heat shock proteins (hsps), including those with molecular weights of 68,000 (hsp 68), 70,000 (hsp 70) and 89,000 (hsp 89). Hyperthermic stresses, which produce the hsps, also cause expression of thermotolerance. The dependence of thermotolerance expression on hsp synthesis was investigated in this mammalian cell line under different heating conditions. Temperature shift experiments showed that hsp synthesis and thermotolerance expression were dependent not only on the absolute hyperthermic temperature, but also on the difference between the initial incubation temperature and the hyperthermic temperature. Small temperature differences which produced no cell killing did not cause detectable synthesis of hsp 68. Increasing the difference of the initial and hyperthermic temperatures reduced cell survival and increased the synthesis of hsp 68. Thermotolerance could be expressed by surviving cells following an initial heat stress even when both heat shock and general protein synthesis were inhibited. Cells exposed to cycloheximide were heated, incubated at their initial temperature for six hours and reheated in the presence of the drug. The inhibitor was then removed and the cells plated for colony formation. The hsps were expressed during this latter incubation period. The regulation of hsp 70 in rat fibroblasts was investigated next. Hsp 70 synthesis rates correlated with the amount of hsp 70 encoding mRNA. The time course of heat shock synthesis and general protein synthesis recovery were each dependent on the duration of the heat stress. Inhibiting protein synthesis with cycloheximide resulted initially in the accumulation of the RNA encoding hsp 70 but did not effect the normal turnover of this RNA species. The conclusions based on these findings are that thermal survival adaptation can be expressed in the absence of hsp 68 synthesis. Hsp 68 is expressed by cells that will ultimately die (see Chapter 2). The hsps do not appear to protect cells against subsequent heat stress. They may function in a repair capacity (see Chapter 3). Hsp 70 expression is primarily regulated by transcription in Rat-1 cells. Hsp 70 does not act to regulate its own turnover (see Chapter 4).
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The role of mesenchyme in early thymic developmentSuniara, Ravinder K. January 2002 (has links)
No description available.
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Studies on the regulation of low density lipoprotein receptors in cultured human fibroblasts.January 1984 (has links)
by Wai-kee Cheung. / Bibliography: leaves 307-332 / Thesis (M.Ph.)--Chinese University of Hong Kong, 1984
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