scholarly journals Overexpression of human cyclin D1 reduces the transforming growth factor beta (TGF-beta) type II receptor and growth inhibition by TGF-beta 1 in an immortalized human esophageal epithelial cell line.

1994 ◽  
Vol 91 (24) ◽  
pp. 11576-11580 ◽  
Author(s):  
A. Okamoto ◽  
W. Jiang ◽  
S. J. Kim ◽  
E. A. Spillare ◽  
G. D. Stoner ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Growth Inhibition ◽  
Cell Line ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Epithelial Cell Line ◽  
Type Ii ◽  
Tgf Beta ◽  
Growth Factor Beta

Selective inhibition of growth-related gene expression in murine keratinocytes by transforming growth factor beta

1988 ◽  
Vol 8 (8) ◽  
pp. 3088-3093
Author(s):  
R J Coffey ◽  
C C Bascom ◽  
N J Sipes ◽  
R Graves-Deal ◽  
B E Weissman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Epithelial Cell ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Epithelial Cell Line ◽  
Tgf Beta ◽  
Growth Factor Beta ◽  
Posttranscriptional Level

Transforming growth factor beta (TGF beta) is a potent inhibitor of epithelial cell proliferation. A nontumorigenic epidermal growth factor (EGF)-dependent epithelial cell line, BALB/MK, is reversibly growth arrested by TGF beta. TGF beta will also abrogate EGF-stimulated mitogenesis of quiescent BALB/MK cells. Increased levels of calcium (greater than 1.0 mM) will induce differentiation in BALB/MK cells; in contrast, TGF beta-mediated growth inhibition does not result in induction of terminal differentiation. In the present study, the effects of TGF beta and calcium on growth factor-inducible gene expression were examined. TGF beta markedly decreased c-myc and KC gene expression in rapidly growing BALB/MK cells and reduced the EGF induction of c-myc and KC in a quiescent population of cells. TGF beta exerted its control over c-myc expression at a posttranscriptional level, and this inhibitory effect was dependent on protein synthesis. TGF beta had no effect on c-fos gene expression, whereas 1.5 mM calcium attenuated EGF-induced c-fos expression in quiescent cells. Expression of beta-actin, however, was slightly increased in both rapidly growing and EGF-restimulated quiescent BALB/MK cells treated with TGF beta. Thus, in this system, TGF beta selectively reduced expression of certain genes associated with cell proliferation (c-myc and KC), and at least part of the TGF beta effect was at a posttranscriptional level.

scholarly journals Selective inhibition of growth-related gene expression in murine keratinocytes by transforming growth factor beta.

1988 ◽  
Vol 8 (8) ◽  
pp. 3088-3093 ◽  
Author(s):  
R J Coffey ◽  
C C Bascom ◽  
N J Sipes ◽  
R Graves-Deal ◽  
B E Weissman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Epithelial Cell ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Epithelial Cell Line ◽  
Tgf Beta ◽  
Growth Factor Beta ◽  
Posttranscriptional Level

Transforming growth factor beta (TGF beta) is a potent inhibitor of epithelial cell proliferation. A nontumorigenic epidermal growth factor (EGF)-dependent epithelial cell line, BALB/MK, is reversibly growth arrested by TGF beta. TGF beta will also abrogate EGF-stimulated mitogenesis of quiescent BALB/MK cells. Increased levels of calcium (greater than 1.0 mM) will induce differentiation in BALB/MK cells; in contrast, TGF beta-mediated growth inhibition does not result in induction of terminal differentiation. In the present study, the effects of TGF beta and calcium on growth factor-inducible gene expression were examined. TGF beta markedly decreased c-myc and KC gene expression in rapidly growing BALB/MK cells and reduced the EGF induction of c-myc and KC in a quiescent population of cells. TGF beta exerted its control over c-myc expression at a posttranscriptional level, and this inhibitory effect was dependent on protein synthesis. TGF beta had no effect on c-fos gene expression, whereas 1.5 mM calcium attenuated EGF-induced c-fos expression in quiescent cells. Expression of beta-actin, however, was slightly increased in both rapidly growing and EGF-restimulated quiescent BALB/MK cells treated with TGF beta. Thus, in this system, TGF beta selectively reduced expression of certain genes associated with cell proliferation (c-myc and KC), and at least part of the TGF beta effect was at a posttranscriptional level.

scholarly journals Transforming growth factor beta suppresses human immunodeficiency virus expression and replication in infected cells of the monocyte/macrophage lineage.

1991 ◽  
Vol 173 (3) ◽  
pp. 589-597 ◽  
Author(s):  
G Poli ◽  
A L Kinter ◽  
J S Justement ◽  
P Bressler ◽  
J H Kehrl ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Growth Factor ◽  
Cell Line ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tgf Beta ◽  
Immunodeficiency Virus ◽  
Growth Factor Beta

The pleiotropic immunoregulatory cytokine transforming growth factor beta (TGF-beta) potently suppresses production of the human immunodeficiency virus (HIV), the causative agent of the acquired immunodeficiency syndrome, in the chronically infected promonocytic cell line U1. TGF-beta significantly (50-90%) inhibited HIV reverse transcriptase production and synthesis of viral proteins in U1 cells stimulated with phorbol myristate acetate (PMA) or interleukin 6 (IL-6). Furthermore, TGF-beta suppressed PMA induction of HIV transcription in U1 cells. In contrast, TGF-beta did not significantly affect the expression of HIV induced by tumor necrosis factor alpha (TNF-alpha). These suppressive effects were not mediated via the induction of interferon alpha (IFN-alpha). TGF-beta also suppressed HIV replication in primary monocyte-derived macrophages infected in vitro, both in the absence of exogenous cytokines and in IL-6-stimulated cultures. In contrast, no significant effects of TGF-beta were observed in either a chronically infected T cell line (ACH-2) or in primary T cell blasts infected in vitro. Therefore, TGF-beta may play a potentially important role as a negative regulator of HIV expression in infected monocytes or tissue macrophages in infected individuals.

Cloning of a growth arrest-specific and transforming growth factor beta-regulated gene, TI 1, from an epithelial cell line

1991 ◽  
Vol 11 (10) ◽  
pp. 5338-5345
Author(s):  
B Kallin ◽  
R de Martin ◽  
T Etzold ◽  
V Sorrentino ◽  
L Philipson
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Lung Epithelial Cells ◽  
Epithelial Cell Line ◽  
Type I ◽  
Tgf Beta ◽  
Protein Synthesis Inhibitors ◽  
Plasminogen Activator Inhibitor 1 ◽  
Growth Factor Beta

By cDNA cloning and differential screening, five genes that are regulated by transforming growth factor beta (TGF beta) in mink lung epithelial cells were identified. A novel membrane protein gene, TI 1, was identified which was downregulated by TGF beta and serum in quiescent cells. In actively growing cells, the TI 1 gene is rapidly and transiently induced by TGF beta, and it is overexpressed in the presence of protein synthesis inhibitors. It appears to be related to a family of transmembrane glycoproteins that are expressed on lymphocytes and tumor cells. The four other genes were all induced by TGF beta and correspond to the genes of collagen alpha type I, fibronectin, plasminogen activator inhibitor 1, and the monocyte chemotactic cell-activating factor (JE gene) previously shown to be TGF beta regulated.

scholarly journals The types II and III transforming growth factor-beta receptors form homo-oligomers.

1994 ◽  
Vol 126 (1) ◽  
pp. 139-154 ◽  
Author(s):  
Y I Henis ◽  
A Moustakas ◽  
H Y Lin ◽  
H F Lodish
Keyword(s):  
Growth Factor ◽  
Cell Surface ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Type Ii ◽  
Tgf Beta ◽  
Double Labeling ◽  
Beta Receptors ◽  
Growth Factor Beta ◽  
In Cells

Affinity-labeling experiments have detected hetero-oligomers of the types I, II, and III transforming growth factor beta (TGF-beta) receptors which mediate intracellular signaling by TGF-beta, but the oligomeric state of the individual receptor types remains unknown. Here we use two types of experiments to show that a major portion of the receptor types II and III forms homo-oligomers both in the absence and presence of TGF-beta. Both experiments used COS-7 cells co-transfected with combinations of these receptors carrying different epitope tags at their extracellular termini. In immunoprecipitation experiments, radiolabeled TGF-beta was bound and cross-linked to cells co-expressing two differently tagged type II receptors. Sequential immunoprecipitations using anti-epitope monoclonal antibodies showed that type II TGF-beta receptors form homo-oligomers. In cells co-expressing epitope-tagged types II and III receptors, a low level of co-precipitation of the ligand-labeled receptors was observed, indicating that some hetero-oligomers of the types II and III receptors exist in the presence of ligand. Antibody-mediated cross-linking studies based on double-labeling immunofluorescence explored co-patching of the receptors at the cell surface on live cells. In cells co-expressing two differently tagged type II receptors or two differently tagged type III receptors, forcing one receptor into micropatches by IgG induced co-patching of the receptor carrying the other tag, labeled by noncross-linking monovalent Fab'. These studies showed that homo-oligomers of the types II and III receptors exist on the cell surface in the absence or presence of TGF-beta 1 or -beta 2. In cells co-expressing types II and III receptors, the amount of heterocomplexes at the cell surface was too low to be detected in the immunofluorescence co-patching experiments, confirming that hetero-oligomers of the types II and III receptors are minor and probably transient species.

Expression of transforming growth factor-beta type II receptor in rat lung is regulated during development

1995 ◽  
Vol 269 (3) ◽  
pp. L419-L426 ◽  
Author(s):  
Y. Zhao ◽  
S. L. Young
Keyword(s):  
Growth Factor ◽  
Blood Vessels ◽  
Lung Tissue ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Fetal Lung ◽  
Type Ii ◽  
Rat Lung ◽  
Tgf Beta ◽  
Growth Factor Beta

Transforming growth factor-beta (TGF-beta) is an autocrine/paracrine growth factor that regulates cell proliferation, differentiation, extracellular matrix production and various other cell functions in the lung. TGF-beta exerts its effects on cells by binding to transmembrane heteromeric serine-threonine kinase receptors. The expression and localization of specific TGF-beta receptors in the lung, however, have not yet been investigated. In the present studies, we isolated a 1,762-base pair cDNA containing the full-length coding sequence for TGF-beta type II receptor (T beta RII) from rat fetal lung with the use of polymerase chain reaction methods. The expression of T beta RII during lung development was examined by Northern analysis. A 5.1-kilobase T beta RII mRNA was detected in rat lung tissue. T beta RII mRNA was expressed in rat fetal lung tissue early in development, increased as development proceeded, reached maximal concentration postnatally, and then decreased to the adult level. The localization of T beta RII in fetal and postnatal rat lung tissue was investigated with the use of in situ hybridization performed with an antisense RNA probe. T beta RII gene was expressed in the mesenchymal tissue and in the epithelial lining of the developing airway at day 16 of gestation. The hybridization signal of T beta RII mRNA was also observed in the adventitial layer of small blood vessels. Expression of T beta RII gene in the developing airway epithelium occurred along a proximal-distal gradient. In postnatal lung, T beta RII mRNA was detected mainly in parenchymal tissues and blood vessels. Expression of T beta RII remained high in the interstitium of interalveolar septa.(ABSTRACT TRUNCATED AT 250 WORDS)

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