Transforming Growth Factor β Inhibits IL-4-Induced Proliferation of Haemopoietic Cell Lines by Interfering with Signal Transduction Mechanisms

1991 ◽  
Vol 80 (s24) ◽  
pp. 3P-3P
Author(s):  
M Wadhwa ◽  
AR Mire-Sluis
Keyword(s):  
Signal Transduction ◽  
Growth Factor ◽  
Cell Lines ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Transduction Mechanisms

scholarly journals Urokinase-type plasminogen activator induces tyrosine phosphorylation of a 78-kDa protein in H-157 cells

1999 ◽  
Vol 277 (2) ◽  
pp. L301-L309 ◽  
Author(s):  
G. Jayarama Bhat ◽  
Jagadambika J. Gunaje ◽  
Steven Idell
Keyword(s):  
Signal Transduction ◽  
Growth Factor ◽  
Plasminogen Activator ◽  
Tyrosine Phosphorylation ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Lung Epithelial Cells ◽  
Upa Receptor ◽  
Type Plasminogen Activator ◽  
Transduction Mechanisms

Studies from our laboratory have shown that exposure of human lung epithelial cells to urokinase plasminogen activator (uPA) induces their proliferation. This effect of uPA is likely to occur via activation of signal transduction pathways. To elucidate uPA-induced signal transduction mechanisms, we exposed H-157 cells to uPA and determined the induced tyrosine phosphorylation profile of proteins. We demonstrate that, in these cells, uPA prominently induced tyrosine phosphorylation of a 78-kDa protein. This effect was observed as early as 30 min and was sustained for at least 24 h. Treatment of cells with agents that abrogate uPA receptor (uPAR) function, including neutralizing anti-uPAR antibody, phosphatidylinositol-specific phospholipase C, or a selective antagonist that blocks the association of uPA with uPAR (Å5 compound), all failed to prevent uPA-induced tyrosine phosphorylation. B-428, an active site inhibitor of uPA activity, prevented the uPA effect. Treatment of cells with hepatocyte growth factor, vascular endothelial growth factor, or transforming growth factor-β, all of which are known to be activated by a uPA-dependent pathway, did not stimulate tyrosine phosphorylation of the 78-kDa protein. uPA induced an increase in [3H]thymidine incorporation into DNA, and cell numbers were unaffected in the presence of Å5. These results demonstrate that, in H-157 cells, uPA induces tyrosine phosphorylation of a 78-kDa protein via a proteolysis-dependent but uPAR-independent mechanism. This novel signaling pathway represents a putative mechanism by which uPA could influence epithelial cell proliferation.

scholarly journals Dual Role for Transforming Growth Factor β-Dependent Signaling in Trypanosoma cruzi Infection of Mammalian Cells

2000 ◽  
Vol 68 (4) ◽  
pp. 2077-2081 ◽  
Author(s):  
Belinda S. Hall ◽  
Miercio A. Pereira
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Trypanosoma Cruzi ◽  
Host Cell ◽  
Cell Lines ◽  
Mammalian Cells ◽  
Transforming Growth Factor ◽  
Growth Arrest ◽  
Transforming Growth Factor Β

ABSTRACT Expression of functional transforming growth factor β (TGF-β) receptors (TβR) is required for the invasion of mammalian cells by the protozoan parasite Trypanosoma cruzi. However, the precise role of this host cell signaling complex in T. cruzi infection is unknown. To investigate the role of the TGF-β signaling pathway, infection levels were studied in the mink lung epithelial cell lines JD1, JM2, and JM3. These cells express inducible mutant TβR1 proteins that cannot induce growth arrest in response to TGF-β but still transmit the signal for TGF-β-dependent gene expression. In the absence of mutant receptor expression, trypomastigotes invaded the cells at a low level. Induction of the mutant receptors caused an increase in infection in all three cell lines, showing that the requirement for TGF-β signaling at invasion can be divorced from TGF-β-induced growth arrest. TGF-β pretreatment of mink lung cells expressing wild-type TβR1 caused a marked enhancement of infection, but no enhancement was seen in JD1, JM2, and JM3 cells, showing that the ability of TGF-β to stimulate infection is associated with growth arrest. Likewise, expression of SMAD7 or SMAD2SA, inhibitors of TGF-β signaling, did not block infection by T. cruzi but did block the enhancement of infection by TGF-β. Taken together, these results show that there is a dual role for TGF-β signaling in T. cruzi infection. The initial invasion of the host cell is independent of both TGF-β-dependent gene expression and growth arrest, but TGF-β stimulation of infection requires a fully functional TGF-β signaling pathway.

scholarly journals NIM811 downregulates transforming growth factor-β signal transduction in vivo and in vitro

2015 ◽  
Vol 13 (1) ◽  
pp. 522-528 ◽  
Author(s):  
JING CHEN ◽  
DIAN-GANG LIU ◽  
HUI WANG ◽  
XIAO-NING WU ◽  
MIN CONG ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β

Transforming growth factor β production by spontaneous malignant mesothelioma cell lines derived from Fisher 344 rats

2001 ◽  
Vol 438 (5) ◽  
pp. 492-497 ◽  
Author(s):  
Maki Kuwahara ◽  
Makio Takeda ◽  
Yukiko Takeuchi ◽  
Masayoshi Kuwahara ◽  
Takanori Harada ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Lines ◽  
Malignant Mesothelioma ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Mesothelioma Cell
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