Fibroblasts cells

The Locomotion of Amoeba The Locomotion of Fibroblastic Cell Types The Locomotion of Leukocytes The Behavior of Locomoting Cells The Role of the Cytoskeleton in Cell Locomotion The Microtubule-Based Cytoskeleton The Intermediate Filament-Based Cytoskeleton The Microfilament-Based Cytoskeleton The Organization of Microfilaments in Cells Microfilament Dynamics and Cell Locomotion Sites of Lamellar Protrusion May Be Determined by the Nucleation of Actin Polymerization... 

Kelley, P.M. Schlesinger, M.J. (1978). The effect of amino acid analogues and heat shock gene expression in chicken embryo fibroblasts. Cell 15, 1277-1286. 

Stock et al. used P4HB scaffolds and tissue engineered the patch with a porosity of 95% and pore sizes in the range of 180-240 p,m by salt-leaching and solvent evaporation. The sheep autologous cells (endothelial, smooth muscle, and fibroblast cells) were seeded on the scaffold before implantation. Results confirmed that the cell-seeded implants induced progressive tissue regeneration with no thrombus formation, stenosis, or dilatation. 

In another study, the original repetitive Cio, (AGAGAGPEG)io, center was reconstructed into nine repeats of AGAGAGPEG with three distributed repeats of the RGD sequence. The new triblock protein, composed of acidic and basic terminal domains in addition to the reconstructed central block, has been shown to support adhesion, spreading, and polarization of human fibroblast cells [82]. Triblock polypeptides that facilitate antibody binding have also been reported [83]. 

Rather scanty evidence exists for the participation of free radicals in Alzheimer s disease and Down s syndrome. However, more recendy, reports have appeared that suggest possible free-radical involvement in the pathogenesis of these two conditions. Zemlan et al. (1989) repotted that the activity of the free-radical scavenging enzyme, SOD, was significantly increased in fibroblast cell lines derived from familial Alzheimer s and Down s patients. They hypothesized that the elevation in SOD activity observed in the Alzheimer patients supports the theory that paired helical filaments are formed by free-radical hydroxylation of proline residues. They further su ested that SOD levels might also be increased in the brains of Alzheimer s and Down s patients, and that the increase in SOD may reflect an enhanced generation of free radicals. 

Flanagan, J. G and Leder, P. (1990). The kit ligand a cell surface molecule altered in Steel mutant fibroblasts. Cell 63 185-194. 

Ratnam, S. and Kent, C. (1995) Early increase in choline kinase-activity upon induction of the H-Ras oncogene in mouse fibroblast cell-lines. Archives of Biochemistry and Biophysics 323, 313—322. 

Kenzelmann M et al. Transcriptome analysis of fibroblast cells immediate-early after human cytomegalovirus infection. J Mol Biol 2000 304 741-751. 

Fig. 5.8 TEM micrographs of fibroblast cells cultured in the absence (A) or presence (B—D) of silica/alginate nanocomposites (Adapted from [34]).

Fizgerald, D., Morris, R.E., and Saclingcr, C.B. (1980) Receptor-mediated internalization of pseudomonas toxin by mouse fibroblasts. Cell 21, 867. 

Glacy, S. (1983) Subcellular distribution of rhodamine-actin microinjected into living fibroblastic cells. Cell Biol. 97, 1207. 

TGF-P was first described as a growth factor capable of inducing transformation of several fibroblast cell lines (hence the name TGFs). It is now recognized that TGF-P actually... 

Fenvalerate inhibits intercellular communication between fibroblast cells and enhances the development of hepatocyte foci in rat liver at nonhepatotoxic dose levels. Chemicals that possess these properties are likely to be tumor promoters (Flodstrom et al. 1988). Fenvalerate alone induced no hepatotoxic effects in rat liver, as judged by transaminase activities and histology. However, some rats that were partially hepatectomized and insulted with nitrosodiethylamine — a carcinogen and tumor initiator — had significantly elevated numbers of liver foci after administrations of fenvalerate. This response suggests that fenvalerate is a potential tumor promoter (Flodstrom et al. 1988). 

The isolation from a marine ascidian and subsequent structure determination of polycitone A (105) (Fig. 6) was first reported [52] by Kashman and coworkers in 1994. In this paper, the penta-O-methyl derivative was reported to inhibit the growth of SV40 transformed fibroblast cells at a concentration of 10 jtg/mL. Loya, Hizi and Kashman published [53] an extensive account of the biological activity of polycitone A in 1999 in which case inhibition of retroviral reverse transcriptases and cellular DNA polymerases was described. The isolation from an ascidian and structure determination of polycitone B (106) (Fig. 4) was subsequently reported [54] by Kashman and coworkers in 2000. Obviously, the presence of extensive bromination in both polycitone A and B make this family of compounds unique among the 3,4-diarylpyrrole natural products. 

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