ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Bradykinin-induced microglial migration mediated by B1-bradykinin receptors depends on Ca2+ influx via reverse-mode activity of the Na+/Ca2+ exchanger.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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58 citing papers in PubMed, 130 citations in OpenAlex.
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- How cell migration helps immune sentinels.Frontiers in cell and developmental biology · 2022Review
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- The Bradykinin B2 Receptor Agonist (NG291) Causes Rapid Onset of Transient Blood-Brain Barrier Disruption Without Evidence of Early Brain Injury.Frontiers in neuroscience · 2021Article
- Ion channels and transporters in microglial function in physiology and brain diseases.Neurochemistry international · 2021Review
- Retinal Physiology and Circulation: Effect of Diabetes.Comprehensive Physiology · 2020Review
- Differential Expression of Kinin Receptors in Human Wet and Dry Age-Related Macular Degeneration Retinae.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Increased plasma bradykinin level is associated with cognitive impairment in Alzheimer's patients.Neurobiology of disease · 2020Article
- Review
- Reciprocal Regulatory Interaction between TRPV1 and Kinin B1 Receptor in a Rat Neuropathic Pain Model.International journal of molecular sciences · 2020Article
- Kinins in Glioblastoma Microenvironment.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2019Article
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18 authors at 5 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Bradykinin (BK) is produced and acts at the site of injury and inflammation. In the CNS, migration of microglia toward the lesion site plays an important role pathologically. In the present study, we investigated the effect of BK on microglial migration. Increased motility of cultured microglia was mimicked by B1 receptor agonists and markedly inhibited by a B1 antagonist but not by a B2 receptor antagonist. BK induced chemotaxis in microglia isolated from wild-type and B2-knock-out mice but not from B1-knock-out mice. BK-induced motility was not blocked by pertussis toxin but was blocked by chelating intracellular Ca2+ or by low extracellular Ca2+, implying that Ca2+ influx is prerequisite. Blocking the reverse mode of Na+/Ca2+ exchanger (NCX) completely inhibited BK-induced migration. The involvement of NCX was further confirmed by using NCX+/- mice; B1-agonist-induced motility and chemotaxis was decreased compared with that in NCX+/+ mice. Activation of NCX seemed to be dependent on protein kinase C and phosphoinositide 3-kinase, and resultant activation of intermediate-conductance (IK-type) Ca2+-dependent K+ currents (I(K(Ca))) was activated. Despite these effects, BK did not activate microglia, as judged from OX6 staining. Using in vivo lesion models and pharmacological injection to the brain, it was shown that microglial accumulation around the lesion was also dependent on B1 receptors and I(K(Ca)). These observations support the view that BK functions as a chemoattractant by using the distinct signal pathways in the brain and, thus, attracts microglia to the lesion site in vivo.
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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.