ArticleJournal of neurochemistry2009
CGRP stimulation of iNOS and NO release from trigeminal ganglion glial cells involves mitogen-activated protein kinase pathways.
Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- A systematic literature review on the role of glial cells in the pathomechanisms of migraine.Frontiers in molecular neuroscience · 2023Pooled it
- Review
- A delayed endothelial-glial mechanism for CGRP-induced migraine.The journal of headache and pain · 2026Review
- Non-neuronal targets for migraine therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Review
- Targeting glial-orchestrated neuroinflammation in migraine pathophysiology.The journal of headache and pain · 2026Review
- Calcitonin gene-related peptide differentially modulates intracellular calcium levels in response to depolarizing stimuli in trigeminal ganglion neurons and glial cells.Neuroscience · 2025Article
- Unraveling the role of CGRP in neurological diseases: a comprehensive exploration to pathological mechanisms and therapeutic implications.Molecular biology reports · 2025Review
- Article
- Method for cryopreservation of trigeminal ganglion for establishing primary cultures of neurons and glia.Journal of neuroscience methods · 2024Article
- Advances in understanding migraine pathophysiology: a bench to bedside review of research insights and therapeutics.Frontiers in molecular neuroscience · 2024Review
- Association of dietary vitamin C consumption with severe headache or migraine among adults: a cross-sectional study of NHANES 1999-2004.Frontiers in nutrition · 2024Article
- The Role of Glial Cells in Different Phases of Migraine: Lessons from Preclinical Studies.International journal of molecular sciences · 2023Review
- Sensory Neuron-TRPV4 Modulates Temporomandibular Disorder Pain Via CGRP in Mice.The journal of pain · 2023Review
- Biomarkers of Migraine: An Integrated Evaluation of Preclinical and Clinical Findings.International journal of molecular sciences · 2023Review
- Grape seed extract suppresses calcitonin gene-related peptide secretion and upregulates expression of GAD 65/67 and GABAB receptor in primary trigeminal ganglion cultures.IBRO neuroscience reports · 2022Article
- [CGRP antibodies in migraine prophylaxis : The new standard in migraine treatment?]Schmerz (Berlin, Germany) · 2022Article
- Corneal neuromediator profiles following laser refractive surgery.Neural regeneration research · 2021Review
- Photophobia: shared pathophysiology underlying dry eye disease, migraine and traumatic brain injury leading to central neuroplasticity of the trigeminothalamic pathway.The British journal of ophthalmology · 2021Review
- Neuropeptides and the Nodes of Ranvier in Cranial Headaches.Frontiers in physiology · 2021Review
- Role of CGRP in Neuroimmune Interaction via NF-κB Signaling Genes in Glial Cells of Trigeminal Ganglia.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Clinical and basic science data support an integral role of calcitonin gene-related peptide (CGRP) in the pathophysiology of temporomandibular joint disorders. Recently, we have shown that CGRP can stimulate the synthesis and release of nitric oxide (NO) from trigeminal ganglion glial cells. The goal of this study was to determine the role of mitogen-activated protein kinase (MAPK) signaling pathways in CGRP regulation of iNOS expression and NO release from cultured trigeminal ganglion glial cells from Sprague-Dawley rats. CGRP treatment for 2 h significantly increased activity of the MAPK reporter genes, Elk, ATF-2, and CHOP. In addition, CGRP increased nuclear staining for the active forms of the MAPKs: extracellular signal-regulated kinase, c-Jun amino-terminal kinase, and p38. This stimulatory event was not observed in cultures pre-treated with the CGRP receptor antagonist peptide CGRP(8-37). Similarly, pre-treatment with selective MAPK inhibitors repressed increases in reporter gene activity as well as CGRP-induced increases in iNOS expression and NO release mediated by MAPKs. In addition, over-expression of MAPK kinase 1 (MEK1), MEK3, MEK6, and MEK kinase significantly increased iNOS expression and NO production in glial cells. Results from our study provide evidence that CGRP binding to its receptor can stimulate iNOS gene expression via activation of MAPK pathways in trigeminal ganglion glial cells.
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Registered trials
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