scholarly journals Involvement of calmodulin and calmodulin kinase II in tumor necrosis factor alpha-induced survival of bone marrow derived macrophages

2012 ◽  
Vol 427 (1) ◽  
pp. 178-184 ◽  
Author(s):  
Jean-Yves Tano ◽  
Robert H. Lee ◽  
Guillermo Vazquez
Keyword(s):  
Bone Marrow ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Calmodulin Kinase ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals In vivo hematopoietic effects of tumor necrosis factor-alpha in normal and erythroleukemic mice: characterization and therapeutic applications

Blood ◽  
1988 ◽  
Vol 72 (6) ◽  
pp. 1875-1883 ◽  
Author(s):  
CS Johnson ◽  
MJ Chang ◽  
P Furmanski
Keyword(s):  
Bone Marrow ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Late Stage ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Abstract The effects of recombinant, macrophage-derived, murine tumor necrosis factor-alpha (TNF-alpha) on hematopoiesis in vivo has been examined in normal mice and in Friend virus (FV)-induced erythroleukemic mice. Intravenous (IV) administration of a single dose of recombinant murine TNF-alpha (10(5) U per mouse) significantly suppressed normal and leukemic late-stage erythropoiesis as measured by numbers of mature erythroid colony forming cells (CFU-E) in the bone marrow and spleen and by peripheral blood reticulocyte counts. In normal animals, the immature erythroid (BFU-E), macrophage (CFU-M), and granulocyte- macrophage (CFU-GM) compartments were significantly stimulated by TNF- alpha in both the bone marrow and the spleen. In the bone marrow of leukemic mice, the BFU-E, CFU-GM, and CFU-M progenitor cell compartments were also stimulated by treatment with the monokine. In the spleens of leukemic mice (the primary site of FV leukemia cell accumulation), relative numbers of BFU-E and CFU-GM were increased by TNF-alpha, while those of CFU-M were suppressed. TNF-alpha caused a rapid decrease in the markedly elevated spleen weights of progressively leukemic mice, and in multiple doses it caused complete clinical disease regression in a significant percentage of leukemic animals. The combination of TNF-alpha with interferon-gamma (IFN-gamma) increased the incidence of leukemia regression, compared with TNF-alpha alone. These results show that TNF-alpha exerts a suppressive influence on late-stage erythropoiesis in vivo and suggest that this effect might be exploited in the treatment of acute erythroleukemia, erythroid hyperplasias, and related diseases.

scholarly journals Synergistic stimulation of macrophage proliferation by the monokines tumor necrosis factor-alpha and colony-stimulating factor 1

Blood ◽  
1989 ◽  
Vol 73 (1) ◽  
pp. 307-311
Author(s):  
DR Branch ◽  
AR Turner ◽  
LJ Guilbert
Keyword(s):  
Bone Marrow ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Bone Marrow Cells ◽  
Human Tumor ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Macrophage Populations ◽  
Necrosis Factor

The effects of pure recombinant human tumor necrosis factor-alpha (TNF) on the CSF-1-stimulated proliferation of well-defined populations of murine macrophages are examined. Primary bone marrow-derived macrophages (BMM) from endotoxin-resistant C3H/HeJ mice were characterized for homogeneity in comparison with a cloned, growth factor-dependent macrophage cell line (S1) also derived from C3H/HeJ bone marrow cells. The mitogenic effects of each factor, alone and in combination, on the proliferation of both macrophage populations over a two-day culture period were studied. In contrast to CSF-1, TNF alone only slightly stimulated macrophage proliferation. However, the combination of CSF-1 and TNF stimulated proliferation of both primary BMM and S1 cells 1.5- to 2-fold greater than the sum of their predicted individual contributions. Such synergy was observed even at very high (plateau) levels of factors. TNF was found to transiently down-regulate CSF-1 receptor levels on both populations. Down-regulation was maximal at one hour; however, receptor numbers returned to initial, or greater, levels after 24 hours of incubation. Thus, TNF, an inducible monokine, greatly enhances the maximal mitogenic effects of CSF-1, an inducer of TNF production. These observations suggest an autocrine rule for TNF that involves synergy with (and perhaps obligatory cooperation with) CSF-1 in the regulation of macrophage proliferation.

scholarly journals Tumor necrosis factor alpha in human bone marrow recipients [letter; comment]

Blood ◽  
1990 ◽  
Vol 76 (12) ◽  
pp. 2639-2640 ◽  
Author(s):  
OS Sardas ◽  
M Beksac ◽  
H Koc ◽  
O Ilhan ◽  
H Akan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Necrosis Factor Alpha ◽  
Letter Comment ◽  
Factor Alpha ◽  
Necrosis Factor
Sign in / Sign up

Export Citation Format

Share Document