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Biomedical subjects

W Scher

Publications and source records attributed to W Scher.

At least 37 records · Page 2Linked to original sources
PubMed1982

DNA ligase and DNase activities in mouse erythroleukemia cells during dimethyl sulfoxide-induced differentiation.

DNA ligase and DNase levels were measured in cell-free extracts from untreated mouse erythroleukemia (MEL) cells and from cells treated with dimethyl sulfoxide (Me2SO) to induce erythroid differentiation. The DNase activity present in the extracts was sensitive to inhibition by G-actin and was, therefore, presumed to be DNase I. When the MEL cells were induced to differentiate by culturing in the presence of 1.8% Me2SO for 3 or 4 days, the apparent activity of the DNA ligase decreased to approximately 12% of the value in untreated MEL cells. In contrast, the apparent DNase I activity of the extracts from Me2SO-treated cells increased over that in extracts from untreated cells by a factor of 2. The activity of acid phosphatase, a lysosomal enzyme, remained unchanged. When strain DR-10, a mutant of the MEL cells which does not undergo Me2SO-induced differentiation, was treated with Me2SO, the DNA ligase and DNase activities of extracts from these cells remained unchanged as compared to extracts from untreated DR-10 cells. Therefore, the marked increase in the level of DNA ligase activity appeared to be related to the process of differentiation in the Me2SO-treated MEL cells.

Animals↗
PubMed1978

Inhibition of dimethyl sulfoxide-stimulated Friend cell erythrodifferentiation by hydrocortisone and other steroids.

Erythrodifferentiation and hemoglobin synthesis in dimethyl sulfoxide-stimulated Friend erythroleukemia cells were inhibited by hydrocortisone (HC) and four other steroids: dexamethasone, deoxycorticosterone, corticosterone, and aldosterone. The effect was specific, because no significant cytotoxicity occurred with any of these compounds at the concentrations that were inhibitory. The mechanism of action of HC was studied in detail. In the absence of dimethyl sulfoxide, it had no effect on hemoglobin levels; but, in the presence of this inducer, the synthesis of heme and globin were each inhibited by approximately 90%. There was no alteration in the synthesis of any major protein other than globin, as determined by gel electrophoresis of cell lysates. The activities of two enzymes in the heme biosynthetic pathway, delta-aminolevulinate dehydratase and uroporphyrinogen-I synthase, were inhibited by 80% and 70%, respectively. Globin mRNA induction was reduced by approximately 90%. This demonstrated that the HC inhibition of globin synthesis occurred at a pretranslational step. The dimethyl sulfoxide-induced single-stranded breaks in DNA, which have been suggested to play a role in Friend leukemia cell differentiation, were reduced in number but not eliminated. HC reduced the dimethyl sulfoxide-stimulation of virus release into the medium by approximately 50%. HC treatment in the absence of dimethyl sulfoxide doubled the production of virus.

Aldosterone↗
PubMed1977

Increased carbonic anhydrase activity in Friend erythroleukemia cells during DMSO-stimulated erythroid differentiation and its inhibition by BrdU.

Carbonic anhydrase activity is increased in Friend erythroleukemia (FL) cells during the enhancement of erythroid differentiation in the presence of dimethylsulfoxide (DMSO) or butyric acid. Untreated FL cells show an increase in enzyme activity associated with logarithmic growth. The increase in the specific activity of carbonic anhydrase in the differentiating treated cells, however, appears to be due to at least two additional general mechanisms: (1) an induction of carbonic anhydrase paralleling the stimulation of hemoglobin synthesis and (2) the stability and/or retention of active carbonic anhydrase as compared to most of the other cell proteins. The stimulation of carbonic anhydrase activity in the treated cells is inhibited by 5-bromo-2'-deoxyuridine (BrdU). This is the first demonstration of BrdU inhibition of a DMSO induced product not directly related to hemoglobin.

Acetazolamide↗
PubMed1973

Effects of 5-bromo-2' -deoxyuridine on production of globin messenger RNA in dimethyl sulfoxide-stimulated Friend leukemia cells.

Friend leukemia cells grown in the presence of dimethyl sulfoxide show enhanced erythroid differentiation and hemoglobin synthesis. The effects of dimethyl sulfoxide stimulation are inhibited by BrdU. To determine the effect of BrdU on the amount of globin mRNA present in cells treated and not treated with dimethyl sulfoxide, molecular hybridization between total cell RNA and [(3)H]DNA complementary to mouse globin mRNA was used. Cells treated with BrdU and dimethyl sulfoxide had 70% less globin mRNA than cells treated with dimethyl sulfoxide alone. The size and base sequence of the residual globin mRNA in the cultures treated with BrdU and dimethyl sulfoxide were unaltered. Cells treated with BrdU alone contained slightly more globin mRNA than did the untreated controls, suggesting that BrdU may have a dual effect in transcription of messenger RNA.

Animals↗
PubMed1971

Hemoglobin synthesis in murine virus-induced leukemic cells in vitro: stimulation of erythroid differentiation by dimethyl sulfoxide.

Cells of a cloned line of murine virus-induced erythroleukemia were stimulated to differentiate along the erythroid pathway by dimethyl sulfoxide at concentrations that did not inhibit growth. A rise in the number of benzidine-positive normoblasts was accompanied by increased synthesis of heme and hemoglobin and a decrease in the malignancy of the cells. This action of dimethyl sulfoxide, which was reversible, may represent the derepression of leukemic cells to permit their maturation.

Animals↗