Expression of Viral and/or Hemoglobin Antigens in Friend Virus Erythroleukemic Cells Treated with Dimethyl Sulfoxide and/or Interferon1

2015 ◽  
pp. 445-447
Author(s):  
C. Ramoni ◽  
G. B. Rossi ◽  
C. Grappelli
Keyword(s):  
Dimethyl Sulfoxide ◽  
Friend Virus ◽  
Erythroleukemic Cells

Enhancment of SCA1 Positive Hematopoietic Progenitors in Polycythemic Mice Inhibits Leukemogenesis

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5245-5245
Author(s):  
Yaacov Ben-David ◽  
Tatiana Usenko ◽  
Mehran Haeri ◽  
Laura Vecchiarelli-Federico ◽  
Josef T. Prchal
Keyword(s):  
Mouse Model ◽  
Inhibitory Effect ◽  
Erythropoietin Receptor ◽  
Friend Virus ◽  
Myeloproliferative Disease ◽  
Pronounced Increase ◽  
Related Disorder ◽  
Gm Csf ◽  
Erythroleukemic Cells

Abstract PV is a myeloproliferative disease, displaying a pronounced increase in the number of erythroid cells. Despite this increase, PV patients exhibit a lower incidence of acute leukemia and in particular erythroleukemia compared to its related disorder CML. In this study we induced erythroleukemia in a mouse model of familiar polycythemia, carrying a truncated form of the human erythropoietin-receptor (Epo-R). Previous studies have shown that these mice develop a disease similar to patients with familiar polycythemia, from whom this gain-of-function receptor was isolated and introduced as transgene. We show that the progression of erythroleukemia induced by Friend virus is significantly delayed in this genetic mouse model of polycythemia. These mice exhibit a massive enrichment of Sca1+/cKit− progenitors and mature immune cells compared to normal mice. Co-transplantation experiments revealed that Sca1+/cKit− progenitors inhibit the robust tumorigenic potential of Sca1−/cKit+ erythroleukemic cells. In order to determine the mechanism of erythroleukemia inhibition, we established cell lines from Sca1+/cKit− cell populations and demonstrated a similar anti-leukemic inhibition in vivo. These cells also express cell surface markers for early B-cells (B220) and macrophages (Mac1), and are able to undergo differentiation into macrophages and dendritic cells following treatment with GM-CSF and IL4. We have shown that these cells also secrete factors that inhibit proliferation of erythroleukemic cells in culture, such as Nitric Oxide (NO). Accordingly, an NO inhibitor can suppress the inhibitory effect of the Sca-1+/cKit−/B220+/Mac1+ cells. To further demonstrate the importance of these leukemic inhibitory cells, we induced a polycythemia in normal mice through administration of Epo. Epo administration delayed the development of Friend virus-induced erythroleukemia and significantly increased the number of leukemic inhibitory Sca1+ cells. Our study also demonstrates a significant increase in the number of leukemic inhibitory cells with anti-proliferative effects in response to Epo and granulocyte macrophage-colony stimulating factor (GM-CSF) stimulation. We therefore propose that administration of Epo and GM-CSF in combination with NO agonistic drugs, as well as the identification of novel drugs that can induce the inhibitory Sca-1+/cKit−/B220+/Mac1+ cells, may lead to improved therapies for the treatment of myelodysplastic syndrome. Together, our results identify Sca-1+/cKit−/B220+/Mac1+ cells as potent cellular inhibitors of leukemia and unravel a potentially novel therapeutic approach.

Presence of spectrin in untreated friend erythroleukemic cells. Its accumulation upon treatment of the cells with dimethyl sulfoxide

1978 ◽  
Vol 97 (3) ◽  
pp. 293-304 ◽  
Author(s):  
Giovanni B. Rossi ◽  
Patrizia Aducci ◽  
Roberto Gambari ◽  
Maurizio Minetti ◽  
Patrizia Vernole
Keyword(s):  
Dimethyl Sulfoxide ◽  
Friend Erythroleukemic Cells ◽  
Erythroleukemic Cells

scholarly journals Membrane-bound redox proteins of the murine Friend virus-induced erythroleukemia cell.

1979 ◽  
Vol 83 (1) ◽  
pp. 231-239 ◽  
Author(s):  
S R Slaughter ◽  
D E Hultquist
Keyword(s):  
Endoplasmic Reticulum ◽  
Cytochrome C ◽  
Dimethyl Sulfoxide ◽  
Reductase Activity ◽  
Cytochrome B5 ◽  
Erythroid Cells ◽  
Friend Virus ◽  
Cytochrome C Reductase ◽  
Membrane Bound ◽  
Nadh Cytochrome

We have obtained and studied a 105,000-g pellet from T-3-Cl-2 cells, a cloned line of Friend virus-induced erythroleukemia cells. By difference spectrophotometry, the pellet was shown to contain cytochrome b5 and cytochrome P-450, hemeproteins that have been shown to participate in electron-transport reactions of endoplasmic reticulum and other membranous fractions of various tissues. The pellet also possesses NADH-cytochrome c reductase activity which is inhibited by anti-cytochrome b5 gamma-globulin, indicating the presence of cytochrome b5 reductase. This is the first demonstration of membrane-bound forms of these redox proteins in erythroid cells. Dimethyl sulfoxide-treated T-3-Cl-2 cells were also shown to possess membrane-bound cytochrome b5 and NADH-cytochrome c reductase activity. We failed to detect soluble cytochrome b5 in the 105,000-g supernatant fraction from homogenates of untreated or dimethyl sulfoxide-treated T-3-Cl-2 cells. In contrast, erythrocytes obtained from mouse blood were shown to possess soluble cytochrome b5 but no membrane-bound form of this protein. These findings are supportive of our hypothesis that soluble cytochrome b5 of erythrocytes is derived from endoplasmic reticulum or some other membrane structure of immature erythroid cells during cell maturation.

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