scholarly journals Modulation of muscarinic-receptor expression in human embryonic lung fibroblasts by platelet-derived growth factor

1990 ◽  
Vol 270 (2) ◽  
pp. 409-412 ◽  
Author(s):  
A Koman ◽  
O Durieu-Trautmann ◽  
P O Couraud ◽  
A D Strosberg ◽  
B B Weksler
Keyword(s):  
Growth Factor ◽  
Binding Capacity ◽  
Human Fibroblasts ◽  
Muscarinic Acetylcholine Receptors ◽  
Receptor Expression ◽  
Regulatory Control ◽  
Platelet Derived Growth Factor ◽  
Lung Fibroblasts ◽  
Human Embryonic Lung ◽  
Rna Levels

Platelet-derived growth factor (PDGF) is known to have regulatory control of a large number of cellular components, including various receptors. We show that muscarinic acetylcholine receptors of the m2 subtype on CCL 137 human fibroblasts in culture are affected by PDGF treatment. A time-dependent down-regulation is observed in steady-state RNA levels, followed by a decrease in ligand-binding capacity. Minimum RNA levels are attained at 11 h; minimum binding capacity is observed after 24 h of treatment. To our knowledge, this is the first example of negative gene control by PDGF.

Expression of recombinant platelet-derived growth factor A- and B-chain homodimers in rat-1 cells and human fibroblasts reveals differences in protein processing and autocrine effects

1988 ◽  
Vol 8 (7) ◽  
pp. 2753-2762
Author(s):  
M Bywater ◽  
F Rorsman ◽  
E Bongcam-Rudloff ◽  
G Mark ◽  
A Hammacher ◽  
...  
Keyword(s):  
Growth Factor ◽  
Human Fibroblasts ◽  
Soft Agar ◽  
Biological Properties ◽  
Platelet Derived Growth Factor ◽  
Cdna Clones ◽  
Metabolic Labeling ◽  
High Saturation ◽  
Dimeric Protein ◽  
A Chain

The autocrine effects of platelet-derived growth factor (PDGF) A- and B-chain homodimers (PDGF-AA and PDGF-BB) on rat-1 cells and human fibroblasts have been investigated by using human PDGF A- and B-chain cDNA clones expressed in a retroviral vector. Infection with replication-defective virus carrying the B-chain cDNA resulted in a phenotypical transformation resembling that induced by simian sarcoma virus. The resulting cells were focus forming in monolayer cultures, grew to high saturation densities, and formed large colonies in soft agar. The PDGF A-chain transfectants showed no transformed morphology and lacked focus-forming activity but grew to high saturation density in monolayer culture and formed small colonies in soft agar. A similar but weaker effect was obtained with an A-chain cDNA variant containing a 69-base-pair insertion in the 3' end of the protein-coding domain. A- and B-chain transfectants released PDGF receptor-competing activity into the medium, but only the medium conditioned by the B-chain transfectants possessed potent mitogenic activity on human fibroblasts. Both types of transfectants had downregulated levels of PDGF receptors; however, the B-chain transfectants were downregulated to significantly lower levels. Metabolic labeling and immunoprecipitations with PDGF antiserum showed that the PDGF B-chain protein was processed to a 24-kilodalton cell-associated and a 30-kilodalton secreted dimeric protein. The A-chain protein was rapidly secreted as a 31-kilodalton dimeric protein. The present study shows a marked difference in the autocrine effects of PDGF-AA and -BB expressed under the control of a retroviral promoter and suggests that different biological properties may be assigned to these two PDGF isoforms.

scholarly journals Imaging of Platelet-Derived Growth Factor Receptor   Expression in Glioblastoma Xenografts Using Affibody Molecule 111In-DOTA-Z09591

2014 ◽  
Vol 55 (2) ◽  
pp. 294-300 ◽  
Author(s):  
V. Tolmachev ◽  
Z. Varasteh ◽  
H. Honarvar ◽  
S. J. Hosseinimehr ◽  
O. Eriksson ◽  
...  
Keyword(s):  
Growth Factor ◽  
Growth Factor Receptor ◽  
Receptor Expression ◽  
Platelet Derived Growth Factor ◽  
Affibody Molecule

scholarly journals Thalidomide inhibits the gene promoter of connective tissue growth factor in human embryonic lung fibroblasts

2020 ◽  
Vol 9 (5) ◽  
pp. 2516-2523
Author(s):  
Yonghui Wu ◽  
Libao Liu ◽  
Jian Zhang ◽  
Lei Huang ◽  
Shaohong Huang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Gene Promoter ◽  
Tissue Growth ◽  
Lung Fibroblasts ◽  
Embryonic Lung ◽  
Human Embryonic Lung

Retinoic acid stimulates immature lung fibroblast growth via a PDGF-mediated autocrine mechanism

2000 ◽  
Vol 279 (1) ◽  
pp. L81-L90 ◽  
Author(s):  
Abraham Liebeskind ◽  
Suseela Srinivasan ◽  
David Kaetzel ◽  
Margaret Bruce
Keyword(s):  
Retinoic Acid ◽  
Growth Factor ◽  
Thymidine Incorporation ◽  
Neutralizing Antibody ◽  
Receptor Expression ◽  
Lung Fibroblasts ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Adult Rat ◽  
Autocrine Mechanism

all trans-retinoic acid (RA) enhances alveolarization in neonates and reinitiates alveolarization in emphysematous adult rat lungs, suggesting that RA may stimulate cell proliferation by upregulating growth factor ligand and/or receptor expression either indirectly or directly by acting on RA-responsive genes encoding growth factors. We report that RA and 1,25-dihydroxyvitamin D3(Vit D), alone and in combination, significantly increase [3H]thymidine incorporation in cultured fetal and postnatal rat lung fibroblasts ( P < 0.05). The greatest increase (11-fold) was seen in 4-day cells treated with the two agents in combination ( P < 0.0001). [3H]thymidine incorporation was age dependent. The greatest response to RA occurred in 4-day fibroblasts ( P < 0.01), whereas the response to Vit D was greatest in embryonic day 20 fibroblasts ( P < 0.001). Neutralizing antibody to platelet-derived growth factor (PDGF)-AB decreased [3H]thymidine incorporation in response to RA alone or in combination with Vit D, indicating a role for PDGF. Expression of mRNAs for PDGF-A and PDGF receptor (PDGFR)-α and -β was upregulated at the transcriptional level in an age- and treatment-dependent manner. Thus exogenous RA may influence alveolarization by stimulating fibroblast proliferation through a PDGF-mediated autocrine mechanism, which is enhanced when RA and Vit D are administered in combination.

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