ArticleJournal of molecular neuroscience : MN2012
Mitogen-activated protein kinase pathways are involved in the upregulation of calcitonin gene-related peptide of rat trigeminal ganglion after organ culture.
Article in Journal of molecular neuroscience : MN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Ictal adipokines are associated with pain severity and treatment response in episodic migraine.Neurology · 2015Trial
- Targeting the microbiome in pediatric migraine: gastrointestinal manifestations and the therapeutic role ofGut microbes · 2026Article
- Sensory Neuron-TRPV4 Modulates Temporomandibular Disorder Pain Via CGRP in Mice.The journal of pain · 2023Review
- Activation of the trigeminal system as a likely target of SARS-CoV-2 may contribute to anosmia in COVID-19.Cephalalgia : an international journal of headache · 2022Article
- TMI-1, TNF-α-Converting Enzyme Inhibitor, Protects Against Paclitaxel-Induced Neurotoxicity in the DRG Neuronal CellsFrontiers in pharmacology · 2022Article
- Identification of Novel Genetic Variants Associated with Insomnia and Migraine Comorbidity.Nature and science of sleep · 2022Article
- Roles of calcitonin gene-related peptide in the skin, and other physiological and pathophysiological functions.Brain, behavior, & immunity - health · 2021Review
- Study on Mechanism of Jiawei Chaiqin Wendan Decoction in Treatment of Vestibular Migraine Based on Network Pharmacology and Molecular Docking Technology.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- The Potentials of Uncariae Ramulus Cum Uncis for the Treatment of Migraine: Targeting CGRP in the Trigeminovascular System.Current neuropharmacology · 2021Review
- ALPK1 missense pathogenic variant in five families leads to ROSAH syndrome, an ocular multisystem autosomal dominant disorder.Genetics in medicine : official journal of the American College of Medical Genetics · 2019Article
- Article
- Review
- Dural administration of inflammatory soup or Complete Freund's Adjuvant induces activation and inflammatory response in the rat trigeminal ganglion.The journal of headache and pain · 2015Article
- New insights into protease-activated receptor 4 signaling pathways in the pathogenesis of inflammation and neuropathic pain: a literature review.Channels (Austin, Tex.) · 2015Review
- Role of c-Jun N-terminal kinase (JNK) activation in micturition reflexes in cyclophosphamide (CYP)-induced cystitis in female rats.Journal of molecular neuroscience : MN · 2014Article
- Role of angiotensin modulation in primary headaches.Current pain and headache reports · 2014Review
- Sex differences in μ-opioid receptor expression in trigeminal ganglia under a myositis condition in rats.European journal of pain (London, England) · 2014Article
- Interleukin-1β increased the expression of protease-activated receptor 4 mRNA and protein in dorsal root ganglion neurons.Neurochemical research · 2013Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The trigeminal ganglion (TG) can express and release calcitonin gene-related peptide (CGRP), an important neuropeptide that plays a crucial role in migraine attack and cluster headache. Activation of rat TG increases CGRP expression. However, the regulatory mechanism of CGRP expression in TG neurons remains to be explored. This study aims to evaluate the involvement of mitogen-activated protein kinase (MAPK) pathways in CGRP upregulation after rat TG organ culture. Rat TG was cultured alone for 24 h or cultured in combination with MAPK inhibitors, tumor necrosis factor α (TNF-α), or interleukin 1β (IL-1β) for 24 h. CGRP protein was determined using immunohistochemistry. The mRNA levels of CGRP, TNF-α, and IL-1β were analyzed through real-time quantitative polymerase chain reaction. MAPK phosphorylation was detected via western blot. After rat TG organ culture, the expressions of CGRP, TNF-α, and IL-1β were upregulated at 24 h. The phosphorylation of extracellular signal-regulated kinases (ERK1/2), P38, and c-jun N-terminal kinases (JNK) significantly increased at 30 min compared with fresh rat TG. In addition, both CGRP expression and phosphorylation of ERK1/2, P38, and JNK were enhanced obviously after rat TG treatment with TNF-α or IL-1β compared with fresh rat TG. However, they decreased markedly after rat TG pretreatment with PD98059 (ERK1/2 inhibitor), SB203580 (P38 inhibitor), or SP600125 (JNK inhibitor) compared with rat TG co-culture with TNF-α or IL-1β. In conclusion, the elevated CGRP expression after rat TG organ culture can be regulated via MAPK pathways. The findings provide insight into the molecular mechanisms and experimental evidence for therapeutic targets of migraine.
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