Regulation of differentiation pathway of skeletal mesenchymal cells in cell lines by transforming growth factor-β superfamily

1995 ◽  
Vol 6 (3) ◽  
pp. 165-173 ◽  
Author(s):  
Akira Yamaguchi
Keyword(s):  
Growth Factor ◽  
Cell Lines ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Mesenchymal Cells

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.

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

scholarly journals Keratinocyte Growth Factor Expression in the Mesenchymal Cells of Human Amnion*

1997 ◽  
Vol 82 (10) ◽  
pp. 3319-3323 ◽  
Author(s):  
M. Linette Casey ◽  
Paul C. MacDonald
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Transforming Growth Factor ◽  
Keratinocyte Growth Factor ◽  
Transforming Growth Factor Β ◽  
Mesenchymal Cells ◽  
Cell Replication ◽  
Human Amnion ◽  
Tetradecanoyl Phorbol Acetate ◽  
Amnion Epithelial Cells

Abstract Amnion epithelial and mesenchymal cells were separated by differential protease treatment, and the separated cells were maintained in monolayer culture. Keratinocyte growth factor (KGF) messenger RNA (mRNA) was readily detected by Northern analysis of amnion mesenchymal cell total RNA (10 μg) but not in amnion epithelial cells. Treatment of the amnion mesenchymal cells in serum-free medium with tetradecanoyl phorbol acetate (1 nm) caused an increase in the level of KGF mRNA. Forskolin treatment also caused an increase in KGF mRNA but not to the levels attained with tetradecanoyl phorbol acetate treatment. Dexamethasone (1 nm) treatment of these cells effected a reduction in the level of KGF mRNA. Prolonged maintenance of mesenchymal cells in serum-free medium also was associated with an increase in the level of KGF mRNA. Treatment with a variety of other agents, viz., interleukin (IL)-1, IL-6 plus or minus IL-6 soluble receptor, IL-11, oncostatin M , epidermal growth factor (EGF), and transforming growth factor-β did not modify the level of KGF mRNA. Treatment of amnion epithelial cells with KGF caused an increase in the rate of [3H]thymidine incorporation, but the rate of cell replication induced by KGF was less than that induced by treatment with EGF. Transforming growth factor-β treatment inhibited basal and EGF- and KGF-stimulated amnion epithelial cell replication. The findings of this study are indicative that KGF is expressed in human amnion mesenchymal cells, and that KGF may act on the epithelial cells of this tissue.

Sign in / Sign up

Export Citation Format

Share Document