ArticleJournal of molecular neuroscience : MN2019
Role of PDGF-A-Activated ERK Signaling Mediated FAK-Paxillin Interaction in Oligodendrocyte Progenitor Cell Migration.
Article in Journal of molecular neuroscience : MN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
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- Platelet-derived growth factor signaling in porcine testicular tubular somatic cells.Cell and tissue research · 2025Article
- Prenatal valproic acid on the basis of gestational diabetes also induces autistic behavior and disrupts myelination and oligodendroglial maturation slightly in offspring.Translational psychiatry · 2025Article
- Choroid plexus apocrine secretion shapes CSF proteome during mouse brain development.Nature neuroscience · 2025Article
- A missense variant in the SOX5 gene (c.221C > T) is associated with intellectual disability.Orphanet journal of rare diseases · 2025Article
- Potential of functional flavonoids in targeting vasospasm through modulation of oxidative stress and SPC-induced signaling pathways.Frontiers in pharmacology · 2025Review
- Targeting PDGF/PDGFR Signaling Pathway by microRNA, lncRNA, and circRNA for Therapy of Vascular Diseases: A Narrow Review.Biomolecules · 2024Review
- Glial Cells as Key Regulators in Neuroinflammatory Mechanisms Associated with Multiple Sclerosis.International journal of molecular sciences · 2024Review
- C-JUN overexpressing CAR-T cells in acute myeloid leukemia: preclinical characterization and phase I trial.Nature communications · 2024Article
- Cellular Components of the Blood-Brain Barrier and Their Involvement in Aging-Associated Cognitive Impairment.Aging and disease · 2024Review
- p38γ MAPK delays myelination and remyelination and is abundant in multiple sclerosis lesions.Brain : a journal of neurology · 2024Article
- The gasdermin family: emerging therapeutic targets in diseases.Signal transduction and targeted therapy · 2024Review
- What Are the Roles of Oligodendrocyte Precursor Cells in Normal and Pathologic Conditions?Neurology · 2023Article
- Brain heterotopia formation by ciliopathic breakdown of neuroepithelial and blood-cerebrospinal fluid barriers.Brain pathology (Zurich, Switzerland) · 2023Article
- Mechanisms of Demyelination and Remyelination Strategies for Multiple Sclerosis.International journal of molecular sciences · 2023Review
- The enigmatic roles of epithelial gasdermin B: Recent discoveries and controversies.Trends in cell biology · 2023Review
- Protocadherin 15 suppresses oligodendrocyte progenitor cell proliferation and promotes motility through distinct signalling pathways.Communications biology · 2022Article
- GSDMB is increased in IBD and regulates epithelial restitution/repair independent of pyroptosis.Cell · 2022Article
- Met is required for oligodendrocyte progenitor cell migration in Danio rerio.G3 (Bethesda, Md.) · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Oligodendrocyte progenitor cells (OPCs) originate from the sub-ventricular zone of the developing brain. They migrate and proliferate to occupy the white matter tracts of the central nervous system and transform into myelinating oligodendrocytes. Along their route of migration, OPCs are guided and controlled by several growth factors and chemokines. PDGF-A (platelet-derived growth factor), a growth factor, serves as a monogenic and mitogenic cue during the process and activates intracellular signaling pathways inside the cell. Activation of extracellular signal regulated kinase (ERK) signaling is one of the mechanisms by which PDGF-A induces the migration of OPCs. However, the mechanisms governing the PDGF-A-induced ERK-driven OPCs migration are still unclear. In the current study, we investigated further the role of PDGF-A-induced ERK signaling in OPC migration. First, we confirmed the role of PDGF-A-activated ERK signaling in OPC migration using the pharmacological inhibitor U0126, or siRNA-mediated suppression of ERK expression. Then, we demonstrated that PDGF-A-induced actin reorganization and interaction of focal adhesion kinase (FAK), Paxillin, and pERK signals are impaired in OPCs treated with the MEK inhibitor U0126. Thus, our findings demonstrated that PDGF-A induces OPC migration in an ERK-dependent mechanism via regulation of actin reorganization and FAK-Paxillin interaction.
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Registered trials
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