scholarly journals Cross-resistance and biochemical studies with two classes of HeLa cell mutants resistant to cardiac glycosides. The unusual behavior of cardenolide SC4453.

1985 ◽  
Vol 260 (11) ◽  
pp. 6843-6850
Author(s):  
R S Gupta ◽  
A Chopra
Keyword(s):  
Hela Cell ◽  
Cardiac Glycosides ◽  
Cross Resistance ◽  
Unusual Behavior ◽  
Biochemical Studies

scholarly journals Up-regulation of FLIP in cisplatin-selected HeLa cells causes cross-resistance to CD95/Fas death signalling

2003 ◽  
Vol 376 (1) ◽  
pp. 253-260 ◽  
Author(s):  
Pachiyappan KAMARAJAN ◽  
Nian-Kang SUN ◽  
Chuck C.-K. CHAO
Keyword(s):  
Cell Surface ◽  
Hela Cell ◽  
Cell Lines ◽  
Antisense Oligonucleotides ◽  
Cross Resistance ◽  
Caspase 8 ◽  
Cervix Carcinoma ◽  
Hela Cell Lines ◽  
Induced Apoptosis ◽  
Resistant Cells

Cisplatin-selected cervix carcinoma HeLa cell lines induced less apoptosis, and weaker activation by cisplatin or Fas-activating antibody, of mitochondrial-associated caspase-9 and death receptor-mediated caspase-8 than did parental cells. Furthermore, less DISC (death-inducing signalling complex) was formed in cisplatin-selected cell lines than in parental cells. Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines. These results imply that cell-surface death signalling is inducible by cisplatin; that reduction of this pathway is associated with drug resistance, and that cisplatin-selected cells acquire cross-resistance to cell-surface death signalling. Sequential up-regulation of FLIP (FLICE-like inhibitory protein), but not Bcl-2, Bcl-xL or inhibitors of apoptosis protein (IAPs), was observed in resistant cells but not in parental cells. The inhibition of FLIP by FLIP antisense oligonucleotides promotes cisplatin and Fas-antibody-induced apoptosis. However, the modulation of apoptosis by FLIP antisense oligonucleotides in resistant cells is greater than that in parental cells. The presented data reveal that the up-regulation of FLIP may contribute to the suppression of apoptosis and thereby change cells that are resistant to cisplatin and Fas-mediated death signals. The results also show that cancer cells that have undergone long-term chemotherapy and become chemoresistant may change the FLIP level, becoming cross-resistant to death factors such as Fas.

Cross-resistance and biochemical characteristics of second-step mutants of HeLa cells resistant to cardiac glycosides

1990 ◽  
Vol 68 (5) ◽  
pp. 852-857
Author(s):  
Arvind Chopra ◽  
Anil K. Dudani ◽  
Radhey S. Gupta
Keyword(s):  
Atpase Activity ◽  
Hela Cells ◽  
Cardiac Glycosides ◽  
Chinese Hamster Ovary Cells ◽  
Mutant Cell ◽  
Chinese Hamster ◽  
Cell Extract ◽  
Cross Resistance ◽  
Second Step ◽  
Ovary Cells

From ouabain-resistant (OuaR) mutants of HeLa cells which do not show any cross resistance to the digoxin analog SC4453, stable second-step mutants resistant to either SC4453 or those exhibiting increased resistance to digoxin have been isolated. The mutants obtained exhibited highly specific cross resistance towards different cardiac glycosides (CGs) and, based on their cross-resistance patterns, contained more than one type of genetic lesion. Biochemical studies with these mutants showed that cellular uptake of 86Rb was inhibited by specific CGs to which they showed increased resistance. The mutants showed reduced binding of [3H]ouabain and [3H]digoxin in comparison with the parental OuaR cells and about 50–60% of the Na+,K+-ATPase activity in the mutant cell extract was highly resistant to inhibition by ouabain and digoxin. In contrast to the above changes, these mutants showed no evidence of amplification, enhanced transcription, or gross alterations in the genes for the α or β subunits of Na+,K+-ATPase. These observations indicated that these mutants involved a second-specific alteration in Na+,K+-ATPase. In contrast to these mutants, Chinese hamster ovary cells, which naturally exhibit comparable levels of resistance to CGs, showed no significant binding of either [3H]ouabain or [3H]digoxin and all of their Na+,K+-ATPase activity was resistant to inhibition by CGs.Key words: cardiac glycosides, mammalian cell mutants, mutants resistant to cardiac glycosides, Na+,Ka+-ATPase.

Ruthenium Red Staining of Human Hard Keratin Fibers

1982 ◽  
Vol 40 ◽  
pp. 278-279
Author(s):  
M. C. Buhrer ◽  
R. A. Mathews
Keyword(s):  
Human Hair ◽  
Ruthenium Red ◽  
Acid Mucopolysaccharides ◽  
Biochemical Studies ◽  
Keratin Fibers ◽  
Ruthenium Red Staining ◽  
Extracellular Materials

Ruthenium red has been used as a stain to demonstrate a variety of extracellular materials, especially acid mucopolysaccharides. It also reacts with certain intracellular and extracellular lipids. Since biochemical studies in our laboratory demonstrated the presence of a variety of monosaccharides in human hair ruthenium red staining procedures were adopted in order to evaluate the presence and morphological location of acid oligosaccharides in the keratinized aspect of hair.

Effects of Hypophysectomy on the Fine Structure of Rat Liver Cells

1967 ◽  
Vol 25 ◽  
pp. 156-157
Author(s):  
Robert R. Cardell
Keyword(s):  
Electron Microscopy ◽  
Fine Structure ◽  
Rat Liver ◽  
Liver Cell ◽  
Anterior Pituitary ◽  
Liver Cells ◽  
Biochemical Studies ◽  
Liver Functions ◽  
Rat Liver Cells ◽  
And Control

Hypophysectomy of the rat renders this animal deficient in the hormones of the anterior pituitary gland, thus causing many primary and secondary hormonal effects on basic liver functions. Biochemical studies of these alterations in the rat liver cell are quite extensive; however, relatively few morphological observations on such cells have been recorded. Because the available biochemical information was derived mostly from disrupted and fractionated liver cells, it seemed desirable to examine the problem with the techniques of electron microscopy in order to see what changes are apparent in the intact liver cell after hypophysectomy. Accordingly, liver cells from rats which had been hypophysectomized 5-120 days before sacrifice were studied. Sham-operated rats served as controls and both hypophysectomized and control rats were fasted 15 hours before sacrifice.

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