Cloning and Characterization of a Novel Transforming Growth Factor-β1-Induced TIAF1 Protein That Inhibits Tumor Necrosis Factor Cytotoxicity

1998 ◽  
Vol 253 (3) ◽  
pp. 743-749 ◽  
Author(s):  
Nan-Shan Chang ◽  
Jeffery Mattison ◽  
Hong Cao ◽  
Nicole Pratt ◽  
Yi Zhao ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Necrosis Factor

Expression of Tumor Necrosis Factor-α and Transforming Growth Factor-β1 in Acute Liver Injury

1989 ◽  
Vol 1 (3) ◽  
pp. 219-226 ◽  
Author(s):  
Mark J. Czaja ◽  
Kathleen C. Flanders ◽  
Luis Biempica ◽  
Charna Klein ◽  
Mark A. Zern ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Liver Injury ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Transforming Growth Factor ◽  
Acute Liver Injury ◽  
Transforming Growth Factor Β1 ◽  
Factor Α ◽  
Necrosis Factor

Retroviral-Mediated Gene Transduction of c-kit Into Single Hematopoietic Progenitor Cells From Cord Blood Enhances Erythroid Colony Formation and Decreases Sensitivity to Inhibition by Tumor Necrosis Factor- and Transforming Growth Factor-β1

Blood ◽  
1999 ◽  
Vol 94 (7) ◽  
pp. 2319-2332 ◽  
Author(s):  
Li Lu ◽  
Michael C. Heinrich ◽  
Li-Sheng Wang ◽  
Mu-Shui Dai ◽  
Amy J. Zigler ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Progenitor Cells ◽  
Colony Formation ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Gm Csf ◽  
Cd34 Cells ◽  
Necrosis Factor

The c-kit receptor and its ligand, steel factor (SLF), are critical for optimal hematopoiesis. We evaluated effects of transducing cord blood (CB) progenitor cells with a retrovirus encoding humanc-kit cDNA. CD34+ cells were sorted as a population or as 1 cell/well for cells expressing high levels of CD34+++ and different levels of c-kit (++, +, Lo/−), transduced and then cultured in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), IL-6, erythropoietin (Epo) +/− SLF in the absence of serum. At a single-cell level, transduction with c-kit, but not with control (neo only), virus significantly increased colony formation, especially by erythroid and multipotential progenitors. The enhancing effect of c-kit transduction was inversely correlated with expression of c-kit protein before transduction. The greatest enhancing effects were noted in CD34+++kitLo/− cells transduced with c-kit. The stimulating effect was apparent even in the absence of exogenously added SLF, but in the presence of GM-CSF, IL-3, IL-6, and Epo. Enzyme-linked immunosorbent assay (ELISA) of SLF protein, reverse transcriptase-polymerase chain reaction (RT-PCR) analysis of SLF mRNA expression in CD34+ cells, and use of neutralizing antibodies to SLF and/or c-kit suggested the presence of endogenous, although probably very low level, expression of SLF by these progenitor cells. Transduction of c-kit significantly decreased sensitivity of progenitor cells to the inhibitory effects of transforming growth factor-β1 and tumor necrosis factor-.c-kit–transduced cells had increased expression ofc-kit protein and decreased spontaneous or cytokine-induced apoptosis. Our results suggest that transduced c-kit into selected progenitor cells can enhance proliferation and decrease apoptosis and that endogenous SLF may mediate this effect.

Soluble tumor necrosis factor (TNF) receptor‐1 induces apoptosis via reverse TNF signaling and autocrine transforming growth factor‐β1

2004 ◽  
Vol 19 (1) ◽  
pp. 91-93 ◽  
Author(s):  
Georg H. Waetzig ◽  
Philip Rosenstiel ◽  
Alexander Arlt ◽  
Andreas Till ◽  
Karen Bräutigam ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Tnf Receptor ◽  
Necrosis Factor
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