Cell fibroblasts, alterations

In light of the increased number of man-6-P/IGF-II receptors in I-cell fibroblasts, the above interactions of IGF could have far-reaching effects. For example, I-cell disease has not been typically associated with abnormalities in phos-phorous/calcium metabolism. The extensive skeletal deformities could involve impairment of mechanisms of orderly calcium deposition. Rather than resulting from a primary disorder of calcium metabolism, it is possible that the bone lesions in I-cell disease are secondary to altered lysosomal processing events in the kidney or liver. 

Milis, D. G. Moore, M. K. Atshaves, B. P Schroeder, F. Jefferson, J. R. Sterol carrier protein-2 expression alters sphingolipid metabolism in transfected mouse L-cell fibroblasts. Mol Cell. Biochem. 2006, 283, 57-66. 

Phosphorothioates generally protect normal tissues more than tumors. Tumor protection reported in some animal studies can pardy be explained by physiological effects of the particular dmgs, which are specific to rodents (4). WR-2721 does not appear to protect human and most animal tumors, apparentiy because of the low availabiUty of the dmg to tumor cells (4). Many tumors appear to have a reduced capillary density (44), which may mean that these tumors have altered levels of alkaline phosphatase, the enzyme that converts WR-2721 to WR-1065. A reduced abiUty of thiols to protect the hypoxic cells characteristic of many tumors may also contribute to their selectivity for normal tissues. The observation that WR-1065 protects cultured normal human fibroblasts, but not fibrosarcoma tumor cells, suggests that additional factors may contribute to the selectivity of radioprotection by WR-2721 m vivo (18). 

In vitro cytotoxicity assays using isolated cells have been applied intermittently to cyanobacterial toxicity testing over several years." Cells investigated for suitability in cyanobacterial toxin assays include primary liver cells (hepatocytes) isolated from rodents and fish, established permanent mammalian cell lines, including hepatocytes, fibroblasts and cancerous cells, and erythrocytes. Earlier work suggested that extracts from toxic cyanobacteria disrupted cells of established lines and erythrocytes," but studies with purified microcystins revealed no alterations in structure or ion transport in fibroblasts or erythrocytes,... 

Arencibia, I., Pedari, L., Sundqvist, K.G. (1987). Induction of motility and alteration of surface membrane polypeptides in lymphocytes by contact with autologous and allogenic fibroblasts. Expt. Cell Res. 172, 124-133. 

Nagasaki, T., Chapin, C.J., Gundersen, G.G. (1992). Distribution of detyrosinated microtubules in motile NRK fibroblasts is rapidly altered upon cell-cell contact Implications for contact inhibition of locomotion. Cell Mot. Cytoskel. 23,45-60. 

Recently, the notion that the chronicity of inflammation may not actually drive the fibrogenic process has been widely appreciated (Tables 1, 2, and 3). Some propose that it is indeed the alteration of the mesenchymal cell phenotypes that disrupts the balance between collagen synthesis and degradation in the wound-healing process, highlighted by clinical evidence that shows unsuccessful treatment of fibrosis with anti-inflammatory or immunosuppressive drugs (18,19). One scenario is that mesenchymal cells (myofibroblasts and fibroblasts) are phenotypically altered and thus do not undergo apoptosis after resolution. 

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

The test is based on an in vitro assay of the uptake of the dye, neutral red (NR), in Balb/c 3T3 fibroblasts. It was developed to detect the phototoxicity induced by the combined interaction of the test substance and light of the wavelength range from 315 to 400 nm, the so-called UVA. The cytotoxicity is evaluated in the presence (+UVA) or absence (-UVA) of UVA light exposure, after application of a nontoxic dose of the compound. The cytotoxicological impact is assessed via the inhibition of the fibroblasts to take up the vital dye NR (NR is a weak cationic dye, penetrating easily into the cell membrane by a nonionic diffusion and accumulates in the lysosomes) one day after the initial treatment. Normally, healthy cells may incorporate and bind NR. Alterations of the cell surface or the lysosomal membranes, however, lead to a decreased uptake and binding of the dye. 

Rogan, E. M., T. M. Bryan, B. Hukku, K. Maclean, A. C. Chang, E. L. Moy, A. Englezou, S. G. Wameford, L. Dalla-Pozza, and R. R. Reddel. 1995. Alterations in p53 and pl6INK4 expression and telomere length during spontaneous immortalization of Li-Fraumeni syndrome fibroblasts. Mol Cell Biol 15(9) 4745-53. 

Basu A, Cline JS (1995) Oncogenic transformation alters cisplatin induced apoptosis in rat embryo fibroblasts. Int J Cancer 63 597-603 Basu A, Weixel KM (1995) Comparison of protein kinase C activity and isoform expression in cisplatin-sensitive and -resistant ovarian carcinoma cells. Int J Cancer 62 457-460... 

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