Calcitriol inhibits growth response to Platelet-Derived Growth Factor-BB in human prostate cells

2005 ◽  
Vol 94 (1-3) ◽  
pp. 189-196 ◽  
Author(s):  
Nadja Nazarova ◽  
Olga Golovko ◽  
Merja Bläuer ◽  
Pentti Tuohimaa
Keyword(s):  
Growth Factor ◽  
Growth Response ◽  
Platelet Derived Growth Factor ◽  
Human Prostate ◽  
Prostate Cells

Patterns of tyrosine phosphorylation differ in vascular hypertrophy and hyperplasia

1994 ◽  
Vol 267 (6) ◽  
pp. C1674-C1681 ◽  
Author(s):  
S. Ali ◽  
G. W. Dorn
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Tyrosine Phosphorylation ◽  
Growth Response ◽  
Thromboxane A2 ◽  
The Other ◽  
Platelet Derived Growth Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Gtpase Activating Protein ◽  
Herbimycin A

Vascular smooth muscle cells (VSMC) undergo hypertrophy when exposed to thromboxane A2 and hyperplasia when exposed to phorbol 12-myristate 13-acetate (PMA) or platelet-derived growth factor (PDGF). Each of these three agonists stimulate rapid tyrosine phosphorylation of numerous VSMC proteins. The current studies were undertaken to identify proteins that are specifically tyrosine phosphorylated in one or the other growth response. All three agonists increased the phosphotyrosine content of multiple proteins. In Western analysis of phosphotyrosine immunoprecipitates, the hyperplastic agents PDGF and PMA increased tyrosine phosphorylation of phospholipase C-gamma 1 (PLC-gamma 1), GTPase-activating protein (GAP), and phosphatidylinositol-3-kinase (PI-3-kinase), while the hypertrophic agonist thromboxane failed to tyrosine-phosphorylate either of these three substrates. Tyrosine kinase inhibition with herbimycin A (5 microM) prevented agonist-stimulated tyrosine phosphorylation of PLC-gamma 1, GAP, and PI-3-kinase. In growth studies, herbimycin A inhibited PMA- and PDGF-induced hyperplasia but not thromboxane-stimulated hypertrophy. These results indicate that tyrosine phosphorylation of PLC-gamma 1, GAP, and PI-3-kinase are specific responses for VSMC hyperplasia but not thromboxane-stimulated hypertrophy.

Stimulation of Hyaluronan Synthetase by Platelet-Derived Growth Factor bb in Human Prostate Smooth Muscle Cells

Pharmacology ◽  
2001 ◽  
Vol 62 (2) ◽  
pp. 103-106 ◽  
Author(s):  
Mark A. Pullen ◽  
Katherine Thomas ◽  
Hsiao-Ling Wu ◽  
Ponnal Nambi
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Platelet Derived Growth Factor ◽  
Human Prostate ◽  
Stimulation Of

Proliferation-Independent Growth Factor Modulation of the Radiation Sensitivity of Human Prostate Cells

1995 ◽  
Vol 143 (2) ◽  
pp. 229 ◽  
Author(s):  
Steven P. Howard ◽  
Kevin M. Groch ◽  
Mary J. Lindstrom ◽  
Edward M. Messing ◽  
Michael N. Gould
Keyword(s):  
Growth Factor ◽  
Radiation Sensitivity ◽  
Human Prostate ◽  
Prostate Cells

Isoform-specific induction of the low-density lipoprotein receptor gene by platelet-derived growth factor

1995 ◽  
Vol 268 (4) ◽  
pp. C1033-C1039 ◽  
Author(s):  
C. Rechtoris ◽  
T. Mazzone
Keyword(s):  
Growth Factor ◽  
Growth Response ◽  
Receptor Gene ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Platelet Derived Growth Factor ◽  
Low Density ◽  
Gene Response ◽  
Myc Gene

We investigated the effect of recombinant platelet-derived growth factor (PDGF) isomers on low-density lipoprotein (LDL) receptor gene expression and compared this with two indexes of cell growth response: expression of the immediate early gene c-myc and the rate of DNA synthesis. In human skin fibroblasts and NIH 3T3 cells, the PDGF-BB homodimer was more effective in inducing the LDL receptor gene and cell growth response compared with the PDGF-AA homodimer. The second messenger pathways utilized by PDGF receptors for enhancing LDL receptor gene response could, however, be dissociated from those utilized for enhancing c-myc gene response and were insensitive to inhibitors of tyrosine phosphorylation. Inhibition of tyrosine kinase activity inhibited c-myc gene response to PDGF-BB at 10(-8) M but had little effect on LDL receptor gene response. Such inhibition increased expression of the LDL receptor gene in the presence of the PDGF-AA isomer. Our results indicate that the response of the LDL receptor gene to PDGF isoforms reflects cellular growth response. However, different transduction pathways are utilized for PDGF activation of the c-myc and LDL receptor genes in mesenchymal cells.

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