ArticleDevelopmental neurobiology2009
ATP and NO dually control migration of microglia to nerve lesions.
Article in Developmental neurobiology, 2009. 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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Who cites it
35 citing papers in PubMed, 66 citations in OpenAlex.
- Time-dependent phenotypical changes of microglia drive alterations in hippocampal synaptic transmission in acute slices.Frontiers in cellular neuroscience · 2024Article
- α-Tocopherol Protects Lipopolysaccharide-Activated BV2 Microglia.Molecules (Basel, Switzerland) · 2023Article
- Activity-dependent oligodendrocyte calcium dynamics and their changes in Alzheimer's disease.Frontiers in cellular neuroscience · 2023Article
- The Interplay between cGMP and Calcium Signaling in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- The Putative Role of Astaxanthin in Neuroinflammation Modulation: Mechanisms and Therapeutic Potential.Frontiers in pharmacology · 2022Review
- Suppression of LPS-Induced Inflammation and Cell Migration by Azelastine through Inhibition of JNK/NF-κB Pathway in BV2 Microglial Cells.International journal of molecular sciences · 2021Article
- Structure versus function: Are new conformations of pannexin 1 yet to be resolved?The Journal of general physiology · 2021Article
- A Novel 1,8-Naphthyridine-2-Carboxamide Derivative Attenuates Inflammatory Responses and Cell Migration in LPS-Treated BV2 Cells via the Suppression of ROS Generation and TLR4/Myd88/NF-κB Signaling Pathway.International journal of molecular sciences · 2021Article
- Inflammatory Cytokine Profile and Plasticity of Brain and Spinal Microglia in Response to ATP and Glutamate.Frontiers in cellular neuroscience · 2021Article
- A Comparative Biology of Microglia Across Species.Frontiers in cell and developmental biology · 2021Review
- Pre-clinical and Clinical Implications of "Inside-Out" vs. "Outside-In" Paradigms in Multiple Sclerosis Etiopathogenesis.Frontiers in cellular neuroscience · 2020Review
- When encephalitogenic T cells collaborate with microglia in multiple sclerosis.Nature reviews. Neurology · 2019Review
- Reformulating Pro-Oxidant Microglia in Neurodegeneration.Journal of clinical medicine · 2019Review
- Extracellular Degradation Into Adenosine and the Activities of Adenosine Kinase and AMPK Mediate Extracellular NADFrontiers in cellular neuroscience · 2018Article
- Nitric Oxide Modulates Postnatal Bone Marrow-Derived Mesenchymal Stem Cell Migration.Frontiers in cell and developmental biology · 2016Article
- ATP release through pannexon channels.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Review
- Minocycline attenuates microglial response and reduces neuronal death after cardiac arrest and cardiopulmonary resuscitation in mice.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015Article
- A Zebrafish Drug-Repurposing Screen Reveals sGC-Dependent and sGC-Independent Pro-Inflammatory Activities of Nitric Oxide.PloS one · 2015Article
- Calreticulin contributes to C1q-dependent recruitment of microglia in the leech Hirudo medicinalis following a CNS injury.Medical science monitor : international medical journal of experimental and clinical research · 2014Article
- Multiple sclerosis: molecular mechanisms and therapeutic opportunities.Antioxidants & redox signaling · 2013Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Microglia migrate rapidly to lesions in the central nervous system (CNS), presumably in response to chemoattractants including ATP released directly or indirectly by the injury. Previous work on the leech has shown that nitric oxide (NO), generated at the lesion, is both a stop signal for microglia at the lesion and crucial for their directed migration from hundreds of micrometers away within the nerve cord, perhaps mediated by a soluble guanylate cyclase (sGC). In this study, application of 100 microM ATP caused maximal movement of microglia in leech nerve cords. The nucleotides ADP, UTP, and the nonhydrolyzable ATP analog AMP-PNP (adenyl-5'-yl imidodiphosphate) also caused movement, whereas AMP, cAMP, and adenosine were without effect. Both movement in ATP and migration after injury were slowed by 50 microM reactive blue 2 (RB2), an antagonist of purinergic receptors, without influencing the direction of movement. This contrasted with the effect of the NO scavenger cPTIO (2-(4-carboxyphenyl)-4,4,5,5-teramethylimidazoline-oxyl-3-oxide), which misdirected movement when applied at 1 mM. The cPTIO reduced cGMP immunoreactivity without changing the immunoreactivity of eNOS (endothelial nitric oxide synthase), which accompanies increased NOS activity after nerve cord injury, consistent with involvement of sGC. Moreover, the sGC-specific inhibitor LY83583 applied at 50 microM had a similar effect, in agreement with previous results with methylene blue. Taken together, the experiments support the hypothesis that ATP released directly or indirectly by injury activates microglia to move, whereas NO that activates sGC directs migration of microglia to CNS lesions.
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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.