Activation of 5-HT7 receptors increases neuronal platelet-derived growth factor β receptor expression

2012 ◽  
Vol 511 (2) ◽  
pp. 65-69 ◽  
Author(s):  
Maryam S. Vasefi ◽  
Jeff S. Kruk ◽  
Hui Liu ◽  
John J. Heikkila ◽  
Michael A. Beazely
Keyword(s):  
Growth Factor ◽  
Receptor Expression ◽  
Platelet Derived Growth Factor ◽  
Β Receptor

scholarly journals Prognostic Significance of Stromal Platelet-Derived Growth Factor β-Receptor Expression in Human Breast Cancer

2009 ◽  
Vol 175 (1) ◽  
pp. 334-341 ◽  
Author(s):  
Janna Paulsson ◽  
Tobias Sjöblom ◽  
Patrick Micke ◽  
Fredrik Pontén ◽  
Göran Landberg ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Human Breast Cancer ◽  
Prognostic Significance ◽  
Receptor Expression ◽  
Platelet Derived Growth Factor ◽  
Human Breast ◽  
Β Receptor

Activated Platelet-Derived Growth Factor β Receptor Expression, P13K-AKT Pathway Molecular Analysis, and Transforming Signals in Equine Sarcoids

2009 ◽  
Vol 46 (4) ◽  
pp. 589-597 ◽  
Author(s):  
G. Borzacchiello ◽  
S. Mogavero ◽  
G. De Vita ◽  
S. Roperto ◽  
L. Della Salda ◽  
...  
Keyword(s):  
Growth Factor ◽  
Normal Skin ◽  
Receptor Expression ◽  
Cyclin D3 ◽  
Platelet Derived Growth Factor ◽  
Regulatory Subunit ◽  
In Vivo Model ◽  
Physical Interaction ◽  
Equine Sarcoid ◽  
Β Receptor

The equine sarcoid is the most common dermatologic neoplasm reported in horses. Bovine papillomavirus (BPV) types 1 and 2 are associated with sarcoids, in which the expression of the major transforming oncoprotein (E5) is often recorded. The transformation activity of the virus is due to the binding of the E5 to the platelet-derived growth factor β receptor (PDGFβ-r). In the present study, we show by Western blot in 4 sarcoid samples and 3 normal equine skin samples that the PDGFβ-r is more phosphorylated in sarcoid tissue than in normal skin ( P < .001). Furthermore, the physical interaction between the activated receptor and the 85-kDa regulatory subunit (p85) of phosphatidylinositol-3-kinase (PI3K) is shown by coimmunoprecipitation. The PI3K-AKT-cyclin D3 molecular pathway downstream to the activation of the PDGFβ-r is shown to be expressed, and the amount of the investigated molecules is higher than normal ( P < .001), suggesting an activation of these effectors in sarcoids. Further, we demonstrate that phospho-JNK and phospho-JUN are more expressed in sarcoids than in normal skin. Our results provide new insights into the pathogenesis of equine sarcoids and support the validity of this in-vivo model to further characterize the molecular pathways underlying BPV E5-induced carcinogenesis.

Role of platelet-derived growth factor in vascular remodeling during pulmonary hypertension in the ovine fetus

2003 ◽  
Vol 284 (5) ◽  
pp. L826-L833 ◽  
Author(s):  
Vivek Balasubramaniam ◽  
Timothy D. Le Cras ◽  
D. Dunbar Ivy ◽  
Theresa R. Grover ◽  
John P. Kinsella ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Remodeling ◽  
Ductus Arteriosus ◽  
Pulmonary Arteries ◽  
Left Pulmonary Artery ◽  
Receptor Expression ◽  
Platelet Derived Growth Factor ◽  
Β Receptor

Platelet-derived growth factor (PDGF) is a potent smooth muscle cell mitogen that may contribute to smooth muscle hyperplasia during the development of chronic pulmonary hypertension (PH). We studied changes in PDGFα- and β-receptor and ligand expression in lambs with chronic intrauterine PH induced by partial ligation of the ductus arteriosus (DA) at gestational age 124–128 days (term = 147 days). Western blot analysis performed on whole lung homogenates from PH animals after 8 days of DA ligation showed a twofold increase in PDGFα- and β-receptor proteins compared with age-matched controls ( P < 0.05). Lung PDGF-A and -B mRNA expression did not differ between PH and control animals. We treated PH animals with NX1975, an aptamer that selectively inhibits PDGF-B, by infusion into the left pulmonary artery for 7 days after DA ligation. NX1975 reduced the development of muscular thickening of small pulmonary arteries by 47% ( P < 0.05) and right ventricular hypertrophy (RVH) by 66% ( P < 0.02). Lung PDGFα- and β-receptor expression is increased in perinatal PH, and NX1975 reduces the increase in wall thickness of small pulmonary arteries and RVH in this model. We speculate that PDGF signaling contributes to structural vascular remodeling in perinatal PH and that selective PDGF inhibition may provide a novel therapeutic strategy for the treatment of chronic PH.

Platelet-Derived Growth Factor Receptor Expression after Neural Grafting in a Rat Model of Parkinson's Disease

1994 ◽  
Vol 3 (6) ◽  
pp. 453-460 ◽  
Author(s):  
Andrea E. Ballagi ◽  
Per Odin ◽  
Agneta Othberg-Cederström ◽  
Anja Smits ◽  
Wei-Ming Duandr ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Growth Factor ◽  
Glial Cells ◽  
Rat Model ◽  
Receptor Expression ◽  
Platelet Derived Growth Factor ◽  
Trophic Effect ◽  
Β Receptor

Platelet-derived growth factor (PDGF) has trophic effect on dopaminergic neurons in vitro. We have previously shown dynamic changes in the expression of PDGF in embryonic mesencephalic grafts and surrounding host striatal tissue following intracerebral transplantation in a rat model of Parkinson's disease. In this study the expression of the PDGF receptors was examined in the same model using immunohistochemistry. Most ventral mesencephalic (VM) cells from E13–E15 rat embryos possessed both PDGF α-and β-receptors before implantation. Double immunofluorescence staining revealed that about 10% of the cells also expressed tyrosine hydroxylase (TH). The PDGF α-receptor was detectable in the graft up to 1 wk after transplantation but had disappeared at 3 wk. In the host tissue, scattered glial cells were positive for the α-receptor but the expression was unchanged following transplantation. The β-receptor expression almost completely disappeared from the grafted tissue by 4 h following transplantation, and only a few cells of the host striatum showed immunoreactivity. However, after 3 wk β-receptor positive cells were again detectable in the graft. These cells appeared to be endothelial cells as identified by an antibody against von Willebrand's factor. Our data suggest that PDGF might act locally on embryonic dopaminergic cells in an autocrine or juxtacrine manner before and shortly after transplantation, and on surrounding glial cells in a paracrine manner after transplantation. Furthermore, PDGF-BB might influence neovascularization in the graft.

Dysregulation of Platelet-Derived Growth Factor β-Receptor Expression by ΔNp73 in Neuroblastoma

2009 ◽  
Vol 7 (12) ◽  
pp. 2031-2039 ◽  
Author(s):  
Daniel Wetterskog ◽  
Abtin Moshiri ◽  
Toshinori Ozaki ◽  
Hidetaka Uramoto ◽  
Akira Nakagawara ◽  
...  
Keyword(s):  
Growth Factor ◽  
Receptor Expression ◽  
Platelet Derived Growth Factor ◽  
Β Receptor

scholarly journals Myc Is an Essential Negative Regulator of Platelet-Derived Growth Factor Beta Receptor Expression

2000 ◽  
Vol 20 (18) ◽  
pp. 6768-6778 ◽  
Author(s):  
Sara K. Oster ◽  
Wilson W. Marhin ◽  
Charlotte Asker ◽  
Linda M. Facchini ◽  
Patrick A. Dion ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Cell Types ◽  
Receptor Expression ◽  
Negative Regulator ◽  
Platelet Derived Growth Factor ◽  
Mrna Levels ◽  
Proliferating Cells ◽  
Receptor Complexes ◽  
Β Receptor

ABSTRACT Platelet-derived growth factor BB (PDGF BB) is a potent mitogen for fibroblasts as well as many other cell types. Interaction of PDGF BB with the PDGF β receptor (PDGF-βR) activates numerous signaling pathways and leads to a decrease in receptor expression on the cell surface. PDGF-βR downregulation is effected at two levels, the immediate internalization of ligand-receptor complexes and the reduction in pdgf-βr mRNA expression. Our studies show that pdgf-βr mRNA suppression is regulated by the c-myc proto-oncogene. Both constitutive and inducible ectopic Myc protein can suppress pdgf-βr mRNA and protein. Suppression of pdgf-βr mRNA in response to Myc is specific, since expression of the related receptorpdgf-αr is not affected. We further show that Myc suppresses pdgf-βr mRNA expression by a mechanism which is distinguishable from Myc autosuppression. Analysis of c-Myc-null fibroblasts demonstrates that Myc is required for the repression of pdgf-βr mRNA expression in quiescent fibroblasts following mitogen stimulation. In addition, it is evident that the Myc-mediated repression of pdgf-βr mRNA levels plays an important role in the regulation of basalpdgf-βr expression in proliferating cells. Thus, our studies suggest an essential role for Myc in a negative-feedback loop regulating the expression of the PDGF-βR.

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