ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Inhibition of the plasma membrane Ca2+ pump by CD44 receptor activation of tyrosine kinases increases the action potential afterhyperpolarization in sensory neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
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- Integrating network pharmacology and transcriptomics to reveal the therapeutic effect of Long Mu Ning Xin Decoction on attention-deficit/hyperactivity disorder by regulating cAMP and PI3K/AKT pathways.Frontiers in pharmacology · 2026Article
- Expression of CD44 and Its Spliced Variants: Innate and Inducible Roles in Nervous Tissue Cells and Their Environment.International journal of molecular sciences · 2025Review
- Article
- Short-Term Benefits from Manual Therapy as an Adjunct Treatment for Persistent Postural-Perceptual Dizziness Symptoms: A Preliminary Prospective Case Series.Journal of functional morphology and kinesiology · 2024Article
- Mechanisms Mediating High-Molecular-Weight Hyaluronan-Induced Antihyperalgesia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Bromelain reversed electrolyte imbalance in the chronically constricted sciatic nerve of Wistar rats.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Primary Active CaCold Spring Harbor perspectives in biology · 2020Review
- CD44 Signaling Mediates High Molecular Weight Hyaluronan-Induced Antihyperalgesia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Evidence for a role of plasma membrane calcium pumps in neurodegenerative disease: Recent developments.Neuroscience letters · 2018Review
- Extracellular matrix hyaluronan signals via its CD44 receptor in the increased responsiveness to mechanical stimulation.Neuroscience · 2016Article
- Ca2+ removal by the plasma membrane Ca2+-ATPase influences the contribution of mitochondria to activity-dependent Ca2+ dynamics in Aplysia neuroendocrine cells.Journal of neurophysiology · 2016Article
- Interleukin-1β activates an Src family kinase to stimulate the plasma membrane Ca2+ pump in hippocampal neurons.Journal of neurophysiology · 2016Article
- CD44: molecular interactions, signaling and functions in the nervous system.Frontiers in cellular neuroscience · 2015Review
- Characterization of silk fibroin modified surface: a proteomic view of cellular response proteins induced by biomaterials.BioMed research international · 2014Article
- Decreases in plasma membrane Ca²⁺-ATPase in brain synaptic membrane rafts from aged rats.Journal of neurochemistry · 2012Article
- Painful nerve injury increases plasma membrane Ca2+-ATPase activity in axotomized sensory neurons.Molecular pain · 2012Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The cytoplasmic Ca(2+) clearance rate affects neuronal excitability, plasticity, and synaptic transmission. Here, we examined the modulation of the plasma membrane Ca(2+) ATPase (PMCA) by tyrosine kinases. In rat sensory neurons grown in culture, the PMCA was under tonic inhibition by a member of the Src family of tyrosine kinases (SFKs). Ca(2+) clearance accelerated in the presence of selective tyrosine kinase inhibitors. Tonic inhibition of the PMCA was attenuated in cells expressing a dominant-negative construct or shRNA directed to message for the SFKs Lck or Fyn, but not Src. SFKs did not appear to phosphorylate the PMCA directly but instead activated focal adhesion kinase (FAK). Expression of constitutively active FAK enhanced and dominant-negative or shRNA knockdown of FAK attenuated tonic inhibition. Antisense knockdown of PMCA isoform 4 removed tonic inhibition of Ca(2+) clearance, indicating that FAK acts on PMCA4. The hyaluronan receptor CD44 activates SFK-FAK signaling cascades and is expressed in sensory neurons. Treating neurons with a CD44-blocking antibody or short hyaluronan oligosaccharides, which are produced during injury and displace macromolecular hyaluronan from CD44, attenuated tonic PMCA inhibition. Ca(2+)-activated K(+) channels mediate a slow afterhyperpolarization in sensory neurons that was inhibited by tyrosine kinase inhibitors and enhanced by knockdown of PMCA4. Thus, we describe a novel kinase cascade in sensory neurons that enables the extracellular matrix to alter Ca(2+) signals by modulating PMCA-mediated Ca(2+) clearance. This signaling pathway may influence the excitability of sensory neurons following injury.
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