ArticleThe Journal of biological chemistry2010
Stimulation of platelet-derived growth factor receptor beta (PDGFRbeta) activates ADAM17 and promotes metalloproteinase-dependent cross-talk between the PDGFRbeta and epidermal growth factor receptor (EGFR) signaling pathways.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- The bone-cerebrovascular axis: effects of bone aging on neurovascular dysfunction and neurodegeneration.The Journal of clinical investigation · 2026Review
- Antagonists of platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) as rationale and therapeutic potential of combination cancer therapy.American journal of clinical and experimental immunology · 2026Review
- Brain Pericytes Enhance MFSD2A Expression and Plasma Membrane Localization in Brain Endothelial Cells Through the PDGF-BB/PDGFRβ Signaling Pathway.International journal of molecular sciences · 2025Article
- ROSBASE1.0: a comprehensive database of reactive oxygen species (ROS): categorization of cell organelles, proteins, taxonomy, and diseases based on ROS-related activities.Database : the journal of biological databases and curation · 2025Article
- Elevated PDGF-BB from Bone Impairs Hippocampal Vasculature by Inducing PDGFRβ Shedding from Pericytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- A Soluble Platelet-Derived Growth Factor Receptor-β Originates via Pre-mRNA Splicing in the Healthy Brain and Is Upregulated during Hypoxia and Aging.Biomolecules · 2023Article
- Normal cerebrospinal fluid concentrations of PDGFRβ in patients with cerebral amyloid angiopathy and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Contribution of ADAM17 and related ADAMs in cardiovascular diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Proteolytic Cleavage of Receptor Tyrosine Kinases.Biomolecules · 2021Review
- Modifications of Plasma Membrane Organization in Cancer Cells for Targeted Therapy.Molecules (Basel, Switzerland) · 2021Review
- Aberrant Expression of a Proliferation-Inducing Ligand Underlies Autoimmune Mechanisms in Immune Thrombocytopenia.Journal of immunology research · 2021Article
- ADAM-Mediated Signalling Pathways in Gastrointestinal Cancer Formation.International journal of molecular sciences · 2020Review
- A novel sensitive assay for detection of a biomarker of pericyte injury in cerebrospinal fluid.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020Article
- Redox control of vascular biology.BioFactors (Oxford, England) · 2020Review
- The pericyte microenvironment during vascular development.Microcirculation (New York, N.Y. : 1994) · 2019Review
- Review
- The RTK Interactome: Overview and Perspective on RTK Heterointeractions.Chemical reviews · 2019Review
- Excess vascular endothelial growth factor-A disrupts pericyte recruitment during blood vessel formation.Angiogenesis · 2019Article
- Blood-brain barrier breakdown is an early biomarker of human cognitive dysfunction.Nature medicine · 2019Article
- SheddomeDB: the ectodomain shedding database for membrane-bound shed markers.BMC bioinformatics · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Binding of the platelet-derived growth factor (PDGF)-B to its receptor PDGFRbeta promotes proliferation, migration, and recruitment of pericytes and smooth muscle cells to endothelial cells, serving to stabilize developing blood vessels. The main goals of this study were to determine whether the extracellular domain of the PDGFRbeta can be proteolytically released from cell membranes and, if so, to identify the responsible sheddase and determine whether activation of the PDGFRbeta stimulates its shedding and potentially that of other membrane proteins. We found that the PDGFRbeta is shed from cells by a metalloproteinase and used loss-of-function experiments to identify ADAM10 as the sheddase responsible for constitutive and ionomycin-stimulated processing of the PDGFRbeta. Moreover, we showed that ligand-dependent activation of the PDGFRbeta does not trigger its own shedding by ADAM10, but instead it stimulates ADAM17 and shedding of substrates of ADAM17, including tumor necrosis factor alpha and transforming growth factor alpha. Finally, we demonstrated that treatment of mouse embryonic fibroblasts with PDGF-B triggers a metalloproteinase-dependent cross-talk between the PDGFRbeta and the epidermal growth factor receptor (EGFR)/ERK1/2 signaling axis that is also critical for PDGF-B-stimulated cell migration, most likely via ADAM17-dependent release and activation of ligands of the EGFR. This study identifies the principal sheddase for the PDGFRbeta and provides new insights into the mechanism of PDGFRbeta-dependent signal transduction and cross-talk with the EGFR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.