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Journal articles on the topic 'PDGFR'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Lesluyes, Tom, Jean-Yves Blay, Patrick Schoffski, et al. "Expression and prognostic significance of PDGF ligands (A, B, C, and D) and PDGFR (A, B, and L) in soft-tissue sarcomas and GIST." Journal of Clinical Oncology 35, no. 15_suppl (2017): 11067. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.11067.

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11067 Background: Sarcomas are a variety of rare connective tissue cancers. Doxorubicin and olaratumab (Ab against PDGFRA) improved survival in a recent Phase 1/2 study. Besides PDGFRA mutated gastrointestinal stroma tumor (GIST) and dermatofibrosarcoma protuberans, the role of PDGFR and the according ligands in the biology of sarcoma remain unclear. Methods: The expression levels of PDGF (A,B,C,D) and PDGFRs (A,B,L) were studied in a series of 255 sarcoma pts in localized phase using the Agilent 014850 platform. Data are available online (http://atg-sarc.sarcomabcb.org). Histologies were GIST

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Lin, Li-Han, Jiun-Sheng Lin, Cheng-Chieh Yang, Hui-Wen Cheng, Kuo-Wei Chang, and Chung-Ji Liu. "Overexpression of Platelet-Derived Growth Factor and Its Receptor Are Correlated with Oral Tumorigenesis and Poor Prognosis in Oral Squamous Cell Carcinoma." International Journal of Molecular Sciences 21, no. 7 (2020): 2360. http://dx.doi.org/10.3390/ijms21072360.

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Oral squamous cell carcinoma (OSCC) is a cancerous disease with poor prognosis. According to the statistics, the 5-year survival rate has not improved significantly over the past 20 years. The platelet-derived growth factor (PDGF) and its signaling pathway is a key regulator of angiogenesis and tumorigenesis. High level of PDGF and its receptor (PDGFR) have been reported in several types of malignancies. In this study, we investigated the relationship of the molecular expression levels of PDGF and PDGFR with clinicopathological parameters in OSCC. To this end, we measured the mRNA and protein

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Ball, Stephen G., Christopher Bayley, C. Adrian Shuttleworth, and Cay M. Kielty. "Neuropilin-1 regulates platelet-derived growth factor receptor signalling in mesenchymal stem cells." Biochemical Journal 427, no. 1 (2010): 29–40. http://dx.doi.org/10.1042/bj20091512.

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Using human MSCs (mesenchymal stem cells) lacking VEGF (vascular endothelial growth factor) receptors, we show that the pro-angiogenic receptor neuropilin-1 associates with phosphorylated PDGFRs [PDGF (platelet-derived growth factor) receptors], thereby regulating cell signalling, migration, proliferation and network assembly. Neuropilin-1 co-immunoprecipitated and co-localized with phosphorylated PDGFRs in the presence of growth factors. Neuropilin-1 knockdown blocked PDGF-AA-induced PDGFRα phosphorylation and migration, reduced PDGF-BB-induced PDGFRβ activation and migration, blocked VEGF-A

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4

Gueller, Saskia, Sigal Gery, and H. Phillip Koeffler. "Adaptor Protein Lnk Binds to PDGFRA, PDGFRB and FIP1L1-PDGFRA, but Not to the TEL-PDGFRB Fusion Protein." Blood 110, no. 11 (2007): 2213. http://dx.doi.org/10.1182/blood.v110.11.2213.2213.

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Abstract PDGFRA and PDGFRB (platelet derived growth factor receptors alpha and beta) are frequently expressed on malignant hematopoietic cells and regulate various cellular responses such as development, proliferation, differentiation, cell survival and cellular transformation. Stimulation by either autocrine loops or constitutional activation by chromosomal translocation (i.e. chronic myelomonocytic leukemia [CMML, TEL-PDGFRB] or chronic eosinophilic leukemia [CEL, FIP1L1-PDGFRA]) makes them important factors in development of hematopoietic disorders. Normally, interaction with the ligand PDG

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5

Kilvaer, Thomas Karsten, Andrej Valkov, Sveinung W. Sorbye, et al. "Platelet-Derived Growth Factors in Non-GIST Soft-Tissue Sarcomas Identify a Subgroup of Patients with Wide Resection Margins and Poor Disease-Specific Survival." Sarcoma 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/751304.

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Background. Optimal treatment of nongastrointestinal stromal tumor soft-tissue sarcomas (non-GIST STSs) is resection with wide margins. This study investigates the prognostic impact of the angiogenesis-associated platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) in non-GIST STS patients with wide and nonwide resection margins.Method. Tumor samples and clinical data from 249 patients with non-GIST STS were obtained, and tissue microarrays were constructed for each specimen. Immunohistochemistry was used to evaluate the expression of PDGF-A, -B, -C, and -D and PDGFR-αand -β.Re

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6

Rogers, Madison A., and Katherine A. Fantauzzo. "The emerging complexity of PDGFRs: activation, internalization and signal attenuation." Biochemical Society Transactions 48, no. 3 (2020): 1167–76. http://dx.doi.org/10.1042/bst20200004.

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The platelet-derived growth factor receptor (PDGFR) family of receptor tyrosine kinases allows cells to communicate with the environment to regulate diverse cellular activities. Here, we highlight recent data investigating the structural makeup of individual PDGFRs upon activation, revealing the importance of the whole receptor in the propagation of extracellular ligand binding and dimerization. Furthermore, we review ongoing research demonstrating the significance of receptor internalization and signal attenuation in the regulation of PDGFR activity. Interactions with internalization machiner

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7

Tsao, Anne S., Nusrat Harun, Junya Fujimoto, et al. "Elevated PDGFRB gene copy number gain as prognostic in resected malignant pleural mesothelioma." Journal of Clinical Oncology 30, no. 15_suppl (2012): 7078. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.7078.

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7078 Background: PDGF/PDGFR pathway has been implicated in malignant pleural mesothelioma (MPM) carcinogenesis. We sought to evaluate the incidence of PDGFRB gene copy number gain (CNG) and PDGFR pathway protein expression by immunohistochemistry (IHC) in the tumor cell cytoplasm, membrane, nucleus, and stroma, and correlate it to patient clinical outcome. Methods: 88 archived tumor blocks from resected MPM with full clinical information were used to perform the analyses. IHC biomarkers for PDGFRα,β and p-PDGFRβ, and fluorescence in situ hybridization were performed for analysis of PDGFRB gene

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8

Fitter, Stephen, Kate Vandyke, Stan Gronthos, and Andrew C. W. Zannettino. "Suppression of PDGF-induced PI3 kinase activity by imatinib promotes adipogenesis and adiponectin secretion." Journal of Molecular Endocrinology 48, no. 3 (2012): 229–40. http://dx.doi.org/10.1530/jme-12-0003.

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Improved glucose and lipid metabolism is a unique side effect of imatinib therapy in some chronic myeloid leukaemia (CML) patients. We recently reported that plasma levels of adiponectin, an important regulator of insulin sensitivity, are elevated following imatinib therapy in CML patients, which could account for these improved metabolic outcomes. Adiponectin is secreted exclusively from adipocytes, suggesting that imatinib modulates adiponectin levels directly, by transcriptional upregulation of adiponectin in pre-existing adipocytes, and/or indirectly, by stimulating adipogenesis. In this r

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9

Kanaan, Rana, and Charlie Strange. "Use of multitarget tyrosine kinase inhibitors to attenuate platelet-derived growth factor signalling in lung disease." European Respiratory Review 26, no. 146 (2017): 170061. http://dx.doi.org/10.1183/16000617.0061-2017.

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Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) play a fundamental role in the embryonic development of the lung. Aberrant PDGF signalling has been documented convincingly in a large variety of pulmonary diseases, including idiopathic pulmonary arterial hypertension, lung cancer and lung fibrosis. Targeting PDGF signalling has been proven to be effective in these diseases. In clinical practice, the most effective way to block PDGF signalling is to inhibit the activity of the intracellular PDGFR kinases. Although the mechanism of action of such drugs is not specific for PDG

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10

Ren, Wenying, Stephanie W. Watts та Barry L. Fanburg. "Serotonin transporter interacts with the PDGFβ receptor in PDGF-BB-induced signaling and mitogenesis in pulmonary artery smooth muscle cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 300, № 3 (2011): L486—L497. http://dx.doi.org/10.1152/ajplung.00237.2010.

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The serotonin transporter (SERT) and the platelet-derived growth factor receptor (PDGFR) have been implicated in both clinical and experimental pulmonary hypertension (PH) and the facilitation of pulmonary artery smooth muscle cell (PASMC) growth. To gain a better understanding of the possible relationship of these two cell surface molecules we have explored interactions between SERT and PDGFR. We have previously demonstrated that SERT transactivates PDGFRβ in serotonin-stimulated PASMC proliferation. We now provide evidence for a role for SERT in PDGF-BB signaling and PASMC proliferation by u

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Thies, Katie, Anisha Hammer, Blake Hildreth та ін. "BSCI-11. STROMAL PLATELET DERIVED GROWTH FACTOR RECEPTOR-β (PDGFRβ) PROMOTES BREAST CANCER BRAIN METASTASIS". Neuro-Oncology Advances 1, Supplement_1 (2019): i3. http://dx.doi.org/10.1093/noajnl/vdz014.009.

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Abstract Stromal platelet-derived growth factor receptor-beta (PDGFRβ) has emerged as an actionable mediator of breast tumor-stromal communication. As a receptor tyrosine kinase, PDGFRβ is activated by its ligand, PDGFB, which is released by neighboring tumor epithelium and endothelium. However, how PDGF signaling mediates breast cancer (BC) initiation, progression, and metastasis remains unclear. To evaluate PDGFRβ in this disease, we developed a mouse model of stromal-specific PDGFRβ activation using the Fsp-cre transgene previously published by our group. Mesenchymal-specific activation of

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12

Zhou, Lingli, Xiaowei Sun, Zijing Huang та ін. "Imatinib Ameliorated Retinal Neovascularization by Suppressing PDGFR-α and PDGFR-β". Cellular Physiology and Biochemistry 48, № 1 (2018): 263–73. http://dx.doi.org/10.1159/000491726.

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Background/Aims: Platelet-derived growth factors (PDGFs) have emerged as pivotal in pathological angiogenesis, which is a hallmark of various tumors and retinal diseases. Here we evaluated the anti-angiogenic effect of imatinib, an inhibitor of PDGF receptors α and β (PDGFR-α and -β), in retinal neovascularization using an oxygen-induced retinopathy (OIR) model. Methods: The OIR model was established and given imatinib or vehicle treatments daily from P12 to P16. At the peak of angiogenesis at P17, the neovascularization area was quantified on retinal whole-mounts with isolectin B4 staining. I

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13

Sugg, Kristoffer B., James F. Markworth, Nathaniel P. Disser, et al. "Postnatal tendon growth and remodeling require platelet-derived growth factor receptor signaling." American Journal of Physiology-Cell Physiology 314, no. 4 (2018): C389—C403. http://dx.doi.org/10.1152/ajpcell.00258.2017.

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Platelet-derived growth factor receptor (PDGFR) signaling plays an important role in the fundamental biological activities of many cells that compose musculoskeletal tissues. However, little is known about the role of PDGFR signaling during tendon growth and remodeling in adult animals. Using the hindlimb synergist ablation model of tendon growth, our objectives were to determine the role of PDGFR signaling in the adaptation of tendons subjected to a mechanical growth stimulus, as well as to investigate the biological mechanisms behind this response. We demonstrate that both PDGFRs, PDGFRα and

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14

Hirst, S. J., P. J. Barnes, and C. H. Twort. "PDGF isoform-induced proliferation and receptor expression in human cultured airway smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 3 (1996): L415—L428. http://dx.doi.org/10.1152/ajplung.1996.270.3.l415.

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The effect of recombinant platelet-derived growth factor (PDGF) isoforms (PDGF-AA, -BB and -AB) on mitogenesis of human cultured airway smooth muscle (ASM) was examined using the MTT-reduction assay and [3H]thymidine incorporation. Results were correlated with expression of PDGF receptor (PDGFR)-alpha and -beta subunits in the absence and presence of fetal calf serum (FCS). When FCS was absent PDGF-AB and -BB were potent mitogens, whereas PDGF-AA was weakly mitogenic, evoking <20% of the maximum response induced by the B-chain isoforms. When FCS (2.5%) was present, all PDGF isoforms stimula

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15

Haley, Stephen, Robert L. Price, Tara A. Bullard, and Louis Terracio. "Platelet-Derived Growth Factor (PDGF) Stimulates Embryonic Cardiac Growth and Myofibrillogenesis." Microscopy and Microanalysis 7, S2 (2001): 1024–25. http://dx.doi.org/10.1017/s1431927600031196.

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Congenital heart disease is a leading cause of death in children with about 40,000 babies born in America each year with congenital heart disease. Common problems include atrial septal defects, patent ductus arteriosus and ventricular septal defects. However, very little is known about the underlying causes of congenital heart disease or the embryonic origin of cardiac malformation. The goal of our recent research has been to examine the role that specific growth factors and their receptors play in the development of the contractile apparatus of the heart and the experiments reported here furt

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16

Johnell, Matilda, Brit Sorensen, Lars Petersen, Carl-Henrik Heldin, and Agneta Siegbahn. "Regulation of chemotaxis by the cytoplasmic domain of tissue factor." Thrombosis and Haemostasis 93, no. 01 (2005): 27–34. http://dx.doi.org/10.1160/th04-07-0405.

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SummaryWe previously demonstrated that FVIIa bound to tissue factor (TF) induces a hyperchemotactic response towards PDGF-BB. The aim of the present study was to investigate the role of the cytoplasmic domain of TF in cell migration. Porcine aortic endothelial (PAE) cells expressing human PDGF β -receptors (PAE/ PDGFR β ) were transfected for expression of human wildtype TF (PAE/PDGFRβ ,TF), a construct lacking the cytoplasmic domain (PAE/PDGFRβ ,TF ∆ cyto), a construct with alanine replacement of serine 258 (PAE/PDGFRβ ,TFS258A), or a construct with alanine replacement of serine 253, 258 and

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Plattner, Rina, Anthony J. Koleske, Andrius Kazlauskas, and Ann Marie Pendergast. "Bidirectional Signaling Links the Abelson Kinases to the Platelet-Derived Growth Factor Receptor." Molecular and Cellular Biology 24, no. 6 (2004): 2573–83. http://dx.doi.org/10.1128/mcb.24.6.2573-2583.2004.

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ABSTRACT The c-Abl nonreceptor tyrosine kinase is activated by growth factor signals such as the platelet-derived growth factor (PDGF) and functions downstream of the PDGF-β receptor (PDGFR) to mediate biological processes such as membrane ruffling, mitogenesis, and chemotaxis. Here, we show that the related kinase Arg is activated downstream of PDGFRs in a manner dependent on Src family kinases and phospholipase C γ1 (PLC-γ1)-mediated phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis, as we showed previously for c-Abl. PIP2, a highly abundant phosphoinositide known to regulate cytoskele

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18

Valius, M., C. Bazenet, and A. Kazlauskas. "Tyrosines 1021 and 1009 are phosphorylation sites in the carboxy terminus of the platelet-derived growth factor receptor beta subunit and are required for binding of phospholipase C gamma and a 64-kilodalton protein, respectively." Molecular and Cellular Biology 13, no. 1 (1993): 133–43. http://dx.doi.org/10.1128/mcb.13.1.133.

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Binding of platelet-derived growth factor (PDGF) to the PDGF receptor (PDGFR) beta subunit triggers receptor tyrosine phosphorylation and the stable association of a number of signal transduction molecules, including phospholipase C gamma (PLC gamma), the GTPase activating protein of ras (GAP), and phosphatidylinositol-3 kinase (PI3K). Previous reports have identified three PDGFR tyrosine phosphorylation sites in the kinase insert domain that are important for stable association of GAP and PI3K. Two of them, tyrosine (Y) 740, and Y-751 are required for the stable association of PI3K, while Y-7

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Valius, M., C. Bazenet, and A. Kazlauskas. "Tyrosines 1021 and 1009 are phosphorylation sites in the carboxy terminus of the platelet-derived growth factor receptor beta subunit and are required for binding of phospholipase C gamma and a 64-kilodalton protein, respectively." Molecular and Cellular Biology 13, no. 1 (1993): 133–43. http://dx.doi.org/10.1128/mcb.13.1.133-143.1993.

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Binding of platelet-derived growth factor (PDGF) to the PDGF receptor (PDGFR) beta subunit triggers receptor tyrosine phosphorylation and the stable association of a number of signal transduction molecules, including phospholipase C gamma (PLC gamma), the GTPase activating protein of ras (GAP), and phosphatidylinositol-3 kinase (PI3K). Previous reports have identified three PDGFR tyrosine phosphorylation sites in the kinase insert domain that are important for stable association of GAP and PI3K. Two of them, tyrosine (Y) 740, and Y-751 are required for the stable association of PI3K, while Y-7

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Ball, Stephen G., C. Adrian Shuttleworth, and Cay M. Kielty. "Vascular endothelial growth factor can signal through platelet-derived growth factor receptors." Journal of Cell Biology 177, no. 3 (2007): 489–500. http://dx.doi.org/10.1083/jcb.200608093.

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Vascular endothelial growth factor (VEGF-A) is a crucial stimulator of vascular cell migration and proliferation. Using bone marrow–derived human adult mesenchymal stem cells (MSCs) that did not express VEGF receptors, we provide evidence that VEGF-A can stimulate platelet-derived growth factor receptors (PDGFRs), thereby regulating MSC migration and proliferation. VEGF-A binds to both PDGFRα and PDGFRβ and induces tyrosine phosphorylation that, when inhibited, results in attenuation of VEGF-A–induced MSC migration and proliferation. This mechanism was also shown to mediate human dermal fibrob

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Lei, Hetian, Cynthia X. Qian, Jinghu Lei, Luis J. Haddock, Shizuo Mukai, and Andrius Kazlauskas. "RasGAP Promotes Autophagy and Thereby Suppresses Platelet-Derived Growth Factor Receptor-Mediated Signaling Events, Cellular Responses, and Pathology." Molecular and Cellular Biology 35, no. 10 (2015): 1673–85. http://dx.doi.org/10.1128/mcb.01248-14.

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Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) make profound contributions to both physiology and pathology. While it is widely believed that direct (PDGF-mediated) activation is the primary mode of activating PDGFRs, the discovery that they can also be activated indirectly begs the question of the relevance of the indirect mode of activating PDGFRs. In the context of a blinding eye disease, indirect activation of PDGFRα results in persistent signaling, which suppresses the level of p53 and thereby promotes viability of cells that drive pathogenesis. Under the same condit

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Reis, Rui M., Albino Martins, Susana A. Ribeiro та ін. "Molecular Characterization of PDGFR-α/PDGF-A and c-KIT/SCF in Gliosarcomas". Analytical Cellular Pathology 27, № 5-6 (2005): 319–26. http://dx.doi.org/10.1155/2005/347863.

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Gliosarcomas are rare and poorly characterized malignant brain tumors that exhibit a biphasic tissue pattern with areas of gliomatous and sarcomatous differentiation. These tumors are histological variants of glioblastoma, displaying a similar genetic profile and dismal prognosis. Up-regulation of PDGFR subfamily of tyrosine kinase members, PDGFR-α and c-Kit, and their intracellular effectors RAS/RAF/MAPK has a crucial role in the cancer development. In addition, signal transduction mediated by activating mutations of c-Kit and PDGFR can be effectively blocked by specific tyrosine kinase inhib

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23

Maudsley, Stuart, A. Musa Zamah, Nadeem Rahman, et al. "Platelet-Derived Growth Factor Receptor Association with Na+/H+ Exchanger Regulatory Factor Potentiates Receptor Activity." Molecular and Cellular Biology 20, no. 22 (2000): 8352–63. http://dx.doi.org/10.1128/mcb.20.22.8352-8363.2000.

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ABSTRACT Platelet-derived growth factor (PDGF) is a potent mitogen for many cell types. The PDGF receptor (PDGFR) is a receptor tyrosine kinase that mediates the mitogenic effects of PDGF by binding to and/or phosphorylating a variety of intracellular signaling proteins upon PDGF-induced receptor dimerization. We show here that the Na+/H+ exchanger regulatory factor (NHERF; also known as EBP50), a protein not previously known to interact with the PDGFR, binds to the PDGFR carboxyl terminus (PDGFR-CT) with high affinity via a PDZ (PSD-95/Dlg/Z0-1 homology) domain-mediated interaction and potent

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Madsen, Christine Vestergaard, Karina Dahl Steffensen, Marianne Waldstrøm, and Anders Jakobsen. "Immunohistochemical Expression of Platelet-Derived Growth Factor Receptors in Ovarian Cancer Patients with Long-Term Follow-Up." Pathology Research International 2012 (September 23, 2012): 1–8. http://dx.doi.org/10.1155/2012/851432.

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Introduction. The well-documented role of the PDGF system in tumor growth and angiogenesis has prompted the development of new biological agents targeting the PDGF system. The aim of the present study was to analyze the expression of the PDGF-receptors in ovarian cancer and to investigate its relation to histopathological parameters and long-term overall survival. Methods. The immunohistochemical expression of PDGFR-α and PDGFR-β was investigated in tumor and stromal cells in 170 patients with histologically verified epithelial ovarian cancer. Results. Almost half of the tumor specimens showed

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Osornio-Vargas, A. R., P. M. Lindroos, P. G. Coin, A. Badgett, N. A. Hernandez-Rodriguez, and J. C. Bonner. "Maximal PDGF-induced lung fibroblast chemotaxis requires PDGF receptor-alpha." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 1 (1996): L93—L99. http://dx.doi.org/10.1152/ajplung.1996.271.1.l93.

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Alteration of the platelet-derived growth factor (PDGF) receptor system could be important in enhancing the mitogenic and chemotactic potential of lung fibroblasts during pulmonary fibrogenesis. We previously reported that interleukin-1 beta (IL-1 beta) upregulates the PDGF receptor-alpha (PDGFR-alpha) gene, and in this study we sought to establish the importance of the PDGFR-alpha relative to the PDGFR-beta in mediating a chemotactic response to PDGF-AA, -AB, and -BB. Pretreatment of fibroblasts for 24 h with IL-1 beta increased chemotaxis to all three PDGF isoforms. IL-1 beta pretreatment ma

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Ding, Wei, Traci R. Knox, Renee C. Tschumper, et al. "Platelet-derived growth factor (PDGF)–PDGF receptor interaction activates bone marrow–derived mesenchymal stromal cells derived from chronic lymphocytic leukemia: implications for an angiogenic switch." Blood 116, no. 16 (2010): 2984–93. http://dx.doi.org/10.1182/blood-2010-02-269894.

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Abstract Malignant cells are capable of influencing the microenvironment in a manner that facilitates tumor cell survival. Bidirectional crosstalk between chronic lymphocytic leukemic (CLL) cells and marrow-derived mesenchymal stromal cells (MSCs) activates both cell types. In this study, we observed that the conditioned medium (CM) obtained from CLL cells was able to induce Akt activation in MSC. Subsequent studies investigated the mechanism of MSC activation mediated by CLL-CM. Platelet-derived growth factor receptors (PDGFRs) were selectively activated in MSCs by CLL-CM and found to be crit

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Shen, Jie, Yoko Ishii, Guihua Xu та ін. "PDGFR-β as a Positive Regulator of Tissue Repair in a Mouse Model of Focal Cerebral Ischemia". Journal of Cerebral Blood Flow & Metabolism 32, № 2 (2011): 353–67. http://dx.doi.org/10.1038/jcbfm.2011.136.

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Although platelet-derived growth factors (PDGFs) and receptors (PDGFRs) are abundantly expressed in the central nervous system, their functions largely remain elusive. We investigated the role of PDGFR-β in tissue responses and functional recovery after photothrombolic middle cerebral artery occlusion (MCAO). In the normal adult mouse brain, PDGFR-β was mainly localized in neurons and in pericyte/vascular smooth muscle cells (PC/vSMCs). From 3 to 28 days after MCAO, postnatally induced systemic PDGFR-β knockout mice (Esr-KO) exhibited the delayed recovery of body weight and behavior, and large

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Kohno, Takashi, Norifumi Urao, Takashi Ashino та ін. "IQGAP1 links PDGF receptor-β signal to focal adhesions involved in vascular smooth muscle cell migration: role in neointimal formation after vascular injury". American Journal of Physiology-Cell Physiology 305, № 6 (2013): C591—C600. http://dx.doi.org/10.1152/ajpcell.00011.2013.

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Platelet-derived growth factor (PDGF) stimulates vascular smooth muscle cell (VSMC) migration and neointimal formation in response to injury. We previously identified IQ-domain GTPase-activating protein 1 (IQGAP1) as a novel VEGF receptor 2 binding scaffold protein involved in endothelial migration. However, its role in VSMC migration and neointimal formation in vivo is unknown. Here we show that PDGF stimulation rapidly promotes IQGAP1 association with PDGF receptor-β (PDGFR) as well as IQGAP1 tyrosine phosphorylation in cultured VSMC. Overexpression or knockdown of IQGAP1 enhances or inhibit

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Valius, M., J. P. Secrist, and A. Kazlauskas. "The GTPase-activating protein of Ras suppresses platelet-derived growth factor beta receptor signaling by silencing phospholipase C-gamma 1." Molecular and Cellular Biology 15, no. 6 (1995): 3058–71. http://dx.doi.org/10.1128/mcb.15.6.3058.

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The beta receptor for platelet-derived growth factor (beta PDGFR) is activated by binding of PDGF and undergoes phosphorylation at multiple tyrosine residues. The tyrosine-phosphorylated receptor associates with numerous SH2-domain-containing proteins which include phospholipase C-gamma 1 (PLC gamma), the GTPase-activating protein of Ras (GAP), the p85 subunit of phosphatidylinositol 3 kinase (PI3K), the phosphotyrosine phosphatase Syp, and several other proteins. Our previous studies indicated that PI3K and PLC gamma were required for relay of the mitogenic signal of beta PDGFR, whereas GAP a

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Li Xia, Zhou, Yang Mo, Ye Jie Yu, and Beng H. Chong. "PDGFR Inhibitor Imatinib May be a Potent Drug in Treating Essential Thrombocythemia." Blood 128, no. 22 (2016): 5470. http://dx.doi.org/10.1182/blood.v128.22.5470.5470.

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Abstract Approximates 80% of essential thrombocythemia (ET) patients carrying JAK2, CALR, MPL mutations. However, there is still 20% of ET patients are negative for all three mutations. Our previous studies have demonstrated that platelet-derived growth factor (PDGF) and its receptor (PDGFR) has a potential effect in the regulation of hematopoiesis and megakaryopoiesis. Therefore, we speculated that PDGF/PDGFR may plays an important role in megakaryocyte/platelet related disease, such as ET. In this study, we found an increase of PDGF-BB and PDGFR expression in ET patients comparing to the nor

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Liu, Chunsheng, Jiachu Li, Xiaoyu Xiang та ін. "PDGF receptor-α promotes TGF-β signaling in hepatic stellate cells via transcriptional and posttranscriptional regulation of TGF-β receptors". American Journal of Physiology-Gastrointestinal and Liver Physiology 307, № 7 (2014): G749—G759. http://dx.doi.org/10.1152/ajpgi.00138.2014.

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Platelet-derived growth factor (PDGF) and transforming growth factor-β (TGF-β) signaling are required for hepatic stellate cell (HSC) activation under pathological conditions such as liver metastatic tumor growth. These two signaling pathways are functionally divergent; PDGF signaling promotes proliferation and migration of HSCs, and TGF-β induces transdifferentiation of quiescent HSCs into myofibroblasts. Although PDGF signaling is implicated in TGF-β-mediated epithelial mesenchymal transition of tumor cells, the role of PDGF receptors in TGF-β activation of HSCs has not been investigated. He

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Popova, Antonia P., J. Kelley Bentley, Tracy X. Cui, et al. "Reduced platelet-derived growth factor receptor expression is a primary feature of human bronchopulmonary dysplasia." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 3 (2014): L231—L239. http://dx.doi.org/10.1152/ajplung.00342.2013.

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Animal studies have shown that platelet-derived growth factor (PDGF) signaling is required for normal alveolarization. Changes in PDGF receptor (PDGFR) expression in infants with bronchopulmonary dysplasia (BPD), a disease of hypoalveolarization, have not been examined. We hypothesized that PDGFR expression is reduced in neonatal lung mesenchymal stromal cells (MSCs) from infants who develop BPD. MSCs from tracheal aspirates of premature infants requiring mechanical ventilation in the first week of life were studied. MSC migration was assessed in a Boyden chamber. Human lung tissue was obtaine

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Battegay, E. J., J. Rupp, L. Iruela-Arispe, E. H. Sage, and M. Pech. "PDGF-BB modulates endothelial proliferation and angiogenesis in vitro via PDGF beta-receptors." Journal of Cell Biology 125, no. 4 (1994): 917–28. http://dx.doi.org/10.1083/jcb.125.4.917.

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To delineate potential angiogenic roles of platelet-derived growth factor (PDGF), we have investigated PDGF and its receptors on bovine aortic endothelial cells that exhibit spontaneous angiogenesis in vitro (angiogenic endothelial cells). Initiation of cord/tube formation by angiogenic endothelial cells required bovine or human serum. Neutralization of PDGF-BB in human serum with a monoclonal anti-PDGF-BB antibody reduced cord/tube formation by 37 +/- 10%, whereas neutralizing anti-PDGF-AA and an IgG isotype-matched control antibody had no effect. DNA synthesis in response to PDGF-BB increase

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Zemskov, Evgeny A., Elena Loukinova, Irina Mikhailenko, Richard A. Coleman, Dudley K. Strickland, and Alexey M. Belkin. "Regulation of Platelet-derived Growth Factor Receptor Function by Integrin-associated Cell Surface Transglutaminase." Journal of Biological Chemistry 284, no. 24 (2009): 16693–703. http://dx.doi.org/10.1074/jbc.m109.010769.

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A functional collaboration between growth factor receptors such as platelet derived growth factor receptor (PDGFR) and integrins is required for effective signal transduction in response to soluble growth factors. However, the mechanisms of synergistic PDGFR/integrin signaling remain poorly understood. Our previous work showed that cell surface tissue transglutaminase (tTG) induces clustering of integrins and amplifies integrin signaling by acting as an integrin binding adhesion co-receptor for fibronectin. Here we report that in fibroblasts tTG enhances PDGFR-integrin association by interacti

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Nemoto, E., S. Kanaya, M. Minamibuchi, and H. Shimauchi. "Cleavage of PDGF Receptor on Periodontal Ligament Cells by Elastase." Journal of Dental Research 84, no. 7 (2005): 629–33. http://dx.doi.org/10.1177/154405910508400709.

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Human leukocyte elastase, a neutrophil serine protease, is considered to be a potential immunoregulatory protease. Since the PDGF receptor (PDGFR) on periodontal ligament (PDL) cells is a crucial element for various functions, such as wound healing in periodontal tissue, we investigated the effect of elastase on the expression of PDGFR on PDL cells by flow cytometry and Western blotting. We found that PDGFR-α disappeared with an increasing dose of elastase, and PDGFR-β was degraded into several fragments. Elastase degraded both receptors on fixed cells, indicating that the degradation resulted

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Karlsson, L., P. Lindahl, J. K. Heath, and C. Betsholtz. "Abnormal gastrointestinal development in PDGF-A and PDGFR-(alpha) deficient mice implicates a novel mesenchymal structure with putative instructive properties in villus morphogenesis." Development 127, no. 16 (2000): 3457–66. http://dx.doi.org/10.1242/dev.127.16.3457.

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Development of the gastrointestinal (GI) tract depends on reciprocal epithelial-mesenchymal cell signaling. Here, we demonstrate a role for platelet-derived growth factor-A (PDGF-A) and its receptor, PDGFR-(alpha), in this process. Mice lacking PDGF-A or PDGFR-(alpha) were found to develop an abnormal GI mucosal lining, including fewer and misshapen villi and loss of pericryptal mesenchyme. Onset of villus morphogenesis correlated with the formation of clusters of PDGFR-(alpha) positive cells, ‘villus clusters’, which remained located at the tip of the mesenchymal core of the growing villus. L

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von Bubnoff, Nikolas, Sivahari P. Gorantla, Richard A. Engh, et al. "Sorafenib and Nilotinib Are Candidates to Overcome Imatinib Resistance in Myeloproliferation with FIP1L1-PDGFRA." Blood 114, no. 22 (2009): 2912. http://dx.doi.org/10.1182/blood.v114.22.2912.2912.

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Abstract Abstract 2912 Poster Board II-888 Constitutively activated variants of PDGFRA, PDGFRB can be found in a subset of patients with myeloid neoplasms associated with eosinophilia. The most common is FIP1L1-PDGFRA (FP). Patients with PDGFR-A and -B rearranged myeloproliferation respond to treatment with imatinib. However, single cases of clinical resistance due to a secondary FP/T674I mutation have been reported. In CML, more than 40 different exchanges have been described that confer imatinib resistance, and sequential treatment with imatinib and novel Abl kinase inhibitors has become rea

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Cain, Jennifer A., Jay L. Grisolano, A. Douglas Laird, and Michael H. Tomasson. "Complete remission of TEL-PDGFRB–induced myeloproliferative disease in mice by receptor tyrosine kinase inhibitor SU11657." Blood 104, no. 2 (2004): 561–64. http://dx.doi.org/10.1182/blood-2003-11-3801.

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Abstract The TEL-PDGFRB fusion oncogene is associated with chronic myelomonocytic leukemia (CMML) and results in the expression of a constitutively active tyrosine kinase. SU11657 is a multitargeted selective inhibitor of class III/V receptor tyrosine kinases, including the platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) receptors KIT and FLT3. SU11657 inhibited TEL/PDGFβR kinase activity at nanomolar concentrations and inhibited TELPDGFRB-mediated factor-independent growth in myeloblastic 32D cells. Daily oral administration of SU11657 at 40 mg/kg suppresse

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Aubert, J. D., S. Hayashi, J. Hards, T. R. Bai, P. D. Pare, and J. C. Hogg. "Platelet-derived growth factor and its receptor in lungs from patients with asthma and chronic airflow obstruction." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 6 (1994): L655—L663. http://dx.doi.org/10.1152/ajplung.1994.266.6.l655.

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The airway walls of patients who have asthma or chronic obstructive pulmonary disease (COPD) are thickened by an increase in the amount of smooth muscle and connective tissue. Platelet-derived growth factor (PDGF) is a candidate cytokine for this increase because it can produce smooth muscle proliferation in vitro. The present study was designed to examine the expression of PDGF and its receptor (PDGFR) in lungs from six asthmatics, six patients with COPD, and six patients with normal lung function. PDGF was immunolocalized to tissue macrophages, but the number of PDGF-positive cells was simil

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Aversa, A., S. Basciani, P. Visca, et al. "Platelet-derived growth factor (PDGF) and PDGF receptors in rat corpus cavernosum: changes in expression after transient in vivo hypoxia." Journal of Endocrinology 170, no. 2 (2001): 395–402. http://dx.doi.org/10.1677/joe.0.1700395.

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Platelet-derived growth factor (PDGF) overactivity has been implicated in atherosclerosis and several fibrotic conditions including lung and kidney fibrosis, liver cirrhosis and myelofibrosis. Low oxygen tension (hypoxia) is a known stimulus for transcriptional induction of PDGF ligand and receptor genes in different tissues. We studied the expression and localization of PDGF-A, PDGF-B, and PDGF receptor (PDGFR)-alpha and -beta subunits in adult rat isolated corpus cavernosum (CC) under generalized transient hypoxia (pO(2) 10%) in comparison with normoxic conditions. Semi-quantitative RT-PCR a

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Luk, Kathryn, Sonja Boatman, Katherine N. Johnson, et al. "Influence of Morphine on Pericyte-Endothelial Interaction: Implications for Antiangiogenic Therapy." Journal of Oncology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/458385.

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Morphine stimulates tumor angiogenesis and cancer progression in mice. We examined if morphine influences endothelial-pericyte interaction via platelet-derived growth factor-BB (PDGF-BB) and PDGF receptor-β(PDGFR-β). Clinically relevant doses of morphine stimulated PDGF-BB secretion from human umbilical vein endothelial cells and activated PDGFR-βand mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) phosphorylation in human pericytes. Thesein vitroeffects of morphine were translated into promotion of tumor angiogenesis in a transgenic mice model of breast cancer

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Lindroos, Pamela M., Yi-Zhe Wang, Annette B. Rice та James C. Bonner. "Regulation of PDGFR-α in rat pulmonary myofibroblasts by staurosporine". American Journal of Physiology-Lung Cellular and Molecular Physiology 280, № 2 (2001): L354—L362. http://dx.doi.org/10.1152/ajplung.2001.280.2.l354.

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Upregulation of the platelet-derived growth factor (PDGF) receptor-α (PDGFR-α) is a mechanism of myofibroblast hyperplasia during pulmonary fibrosis. We previously identified interleukin (IL)-1β as a major inducer of the PDGFR-α in rat pulmonary myofibroblasts in vitro. In this study, we report that staurosporine, a broad-spectrum kinase inhibitor, upregulates PDGFR-α gene expression and protein. A variety of other kinase inhibitors did not induce PDGFR-α expression. Staurosporine did not act via an IL-1β autocrine loop because the IL-1 receptor antagonist protein did not block staurosporine-i

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Ricono, Jill M., Brent Wagner, Yves Gorin та ін. "PDGF receptor-β modulates metanephric mesenchyme chemotaxis induced by PDGF AA". American Journal of Physiology-Renal Physiology 296, № 2 (2009): F406—F417. http://dx.doi.org/10.1152/ajprenal.90368.2008.

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PDGF B chain or PDGF receptor (PDGFR)-β-deficient (−/−) mice lack mesangial cells. To study responses of α- and β-receptor activation to PDGF ligands, metanephric mesenchymal cells (MMCs) were established from embryonic day E11.5 wild-type (+/+) and −/− mouse embryos. PDGF BB stimulated cell migration in +/+ cells, whereas PDGF AA did not. Conversely, PDGF AA was chemotactic for −/− MMCs. The mechanism by which PDGFR-β inhibited AA-induced migration was investigated. PDGF BB, but not PDGF AA, increased intracellular Ca2+ and the production of reactive oxygen species (ROS) in +/+ cells. Transfe

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Schneider, Linda, Christian-Martin Stock, Peter Dieterich та ін. "The Na+/H+ exchanger NHE1 is required for directional migration stimulated via PDGFR-α in the primary cilium". Journal of Cell Biology 185, № 1 (2009): 163–76. http://dx.doi.org/10.1083/jcb.200806019.

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We previously demonstrated that the primary cilium coordinates platelet-derived growth factor (PDGF) receptor (PDGFR) α–mediated migration in growth-arrested fibroblasts. In this study, we investigate the functional relationship between ciliary PDGFR-α and the Na+/H+ exchanger NHE1 in directional cell migration. NHE1 messenger RNA and protein levels are up-regulated in NIH3T3 cells and mouse embryonic fibroblasts (MEFs) during growth arrest, which is concomitant with cilium formation. NHE1 up-regulation is unaffected in Tg737orpk MEFs, which have no or very short primary cilia. In growth-arres

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Basciani, Sabrina, Gabriele De Luca, Susanna Dolci та ін. "Platelet-Derived Growth Factor Receptor β-Subtype Regulates Proliferation and Migration of Gonocytes". Endocrinology 149, № 12 (2008): 6226–35. http://dx.doi.org/10.1210/en.2008-0349.

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Proliferation and migration of gonocytes, the precursors of spermatogonial stem cells, to the germline niche in the basal membrane of the seminiferous tubules, are two crucial events that take place between postnatal d 0.5 (P0.5) and P5.0 in the mouse and involve a selection of the cells that are committed to the germline stem cells lineage. Here we show that from embryonic d 18.0 (E18) and up to P5, the gonocytes express platelet-derived growth factor (PDGF) receptor β-subtype (PDGFR-β) and that during the same time period, the Sertoli cells express PDGF-B and PDGF-D, both ligands for PDGFR-β

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Cartel, Nicholas J., Jason Liu, Jinxia Wang та Martin Post. "PDGF-BB-mediated activation of p42MAPK is independent of PDGF β-receptor tyrosine phosphorylation". American Journal of Physiology-Lung Cellular and Molecular Physiology 281, № 4 (2001): L786—L798. http://dx.doi.org/10.1152/ajplung.2001.281.4.l786.

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Herein, we investigated the activity of mitogen-activated protein kinase (MAPK), a key component of downstream signaling events, which is activated subsequent to platelet-derived growth factor (PDGF)-BB stimulation. Specifically, p42MAPK activity peaked 60 min after addition of PDGF-BB, declined thereafter, and was determined not to be a direct or necessary component of glycosaminoglycan (GAG) synthesis. PDGF-BB also activated MAPK kinase 2 (MAPKK2) but had no effect on MAPKK1 and Raf-1 activity. Chemical inhibition of Janus kinase, phosphatidylinositol 3-kinase, Src kinase, or tyrosine phosph

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McGowan, Stephen E., та Diann M. McCoy. "Platelet-derived growth factor receptor-α and Ras-related C3 botulinum toxin substrate-1 regulate mechano-responsiveness of lung fibroblasts". American Journal of Physiology-Lung Cellular and Molecular Physiology 313, № 6 (2017): L1174—L1187. http://dx.doi.org/10.1152/ajplung.00185.2017.

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Platelet-derived growth factor (PDGF)-A, which only signals through PDGF-receptor-α (PDGFR-α), is required for secondary alveolar septal formation. Although PDGFR-α distinguishes mesenchymal progenitor cells during the saccular stage, PDGFR-α-expressing alveolar cells persist through adulthood. PDGF-A sustains proliferation, limits apoptosis, and maintains α-smooth muscle actin (α-SMA)-containing alveolar cells, which congregate at the alveolar entry ring at postnatal day (P)12. PDGFR-α-expressing, α-SMA-containing alveolar cells redistribute in the elongating septum, suggesting that they migr

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Jiang, Zhiyuan, Guoqiang Zhong, Lina Wen та ін. "The Role of Platelet-Derived Growth Factor-B/Platelet-Derived Growth Factor Receptor-β Signaling in Chronic Atrial Fibrillation". Cardiology 133, № 4 (2016): 242–56. http://dx.doi.org/10.1159/000442940.

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Objective: To explore the role of platelet-derived growth factor-B (PDGF-B)/platelet-derived growth factor receptor-β (PDGFR-β) signaling in chronic atrial fibrillation (AF). Methods: Thirty-nine AF patients and 33 patients with sinus rhythm (SR) were enrolled. Twenty canines were randomized into 5 groups: control, sham and AF lasting 1, 2 or 4 weeks. The AF canine models were made by rapid atrial pacing. Rat atrial fibroblasts were treated with PDGF-BB or PDGF-BB + PDGFR inhibitor AG1295, respectively. Gene expression in the right atrial appendage of patients, the left atrium of canines and r

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Rolny, Charlotte, Ingrid Nilsson, Peetra Magnusson та ін. "Platelet-derived growth factor receptor-β promotes early endothelial cell differentiation". Blood 108, № 6 (2006): 1877–86. http://dx.doi.org/10.1182/blood-2006-04-014894.

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AbstractPlatelet-derived growth factor BB (PDGF-BB) has been assigned a critical role in vascular stability by promoting the recruitment of PDGF receptor-β–expressing perivascular cells. Here we present data indicating that early hematopoietic/endothelial (hemangio) precursors express PDGFR-β based on coexpression with CD31, vascular endothelial growth factor receptor-2, and CD41 in 2 models: mouse yolk sac (embryonic day 8 [E8]) and differentiating mouse embryonic stem cells (embryoid bodies). Expression of PDGFR-β on hemangioprecursor cells in the embryoid bodies gradually disappeared, and,

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Ustach, Carolyn V., and Hyeong-Reh Choi Kim. "Platelet-Derived Growth Factor D Is Activated by Urokinase Plasminogen Activator in Prostate Carcinoma Cells." Molecular and Cellular Biology 25, no. 14 (2005): 6279–88. http://dx.doi.org/10.1128/mcb.25.14.6279-6288.2005.

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ABSTRACT Platelet-derived growth factor (PDGF) protein family members are potent mitogens and chemoattractants for mesenchymal cells. The classic PDGF ligands A and B are single-domain protein chains which are secreted as active dimers capable of activating their cognate PDGF receptors (PDGFRs). In contrast to PDGFs A and B, PDGF D contains an N-terminal complement subcomponent C1r/C1s, Uegf, and Bmp1 (CUB) domain and a C-terminal PDGF domain. PDGF D must undergo extracellular proteolytic processing, separating the CUB domain from the PDGF domain, before the PDGF domain can stimulate β-PDGFR-m

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