Tumor Necrosis Factor-alpha Stimulation of Calcitonin Gene-related Peptide Expression and Secretion from Rat Trigeminal Ganglion Neurons.
From: Department of Biology, Missouri State University, Springfield, Missouri 65897, USA.
Journal of neurochemistry
- Publish Date: Jan 2006
- ISSN: 0022-3042
- Volume: 96
- Issue: 1
- Pages: 65-77
- Medium: Print
- Language: English
- Citation (JAMA): Bowen Elizabeth J, Schmidt Thomas W, Firm Christina S, et al. Tumor Necrosis Factor-alpha Stimulation of Calcitonin Gene-related Peptide Expression and Secretion from Rat Trigeminal Ganglion Neurons.. J. Neurochem. Jan 2006;96:65-77
Abstract
Expression of the neuropeptide calcitonin gene-related peptide (CGRP) in trigeminal ganglion is implicated in neurovascular headaches and temporomandibular joint disorders. Elevation of cytokines contributes to the pathology of these diseases. However, a connection between cytokines and CGRP gene expression in trigeminal ganglion nerves has not been established. We have focused on the effects of the cytokine tumor necrosis factor-alpha (TNF-alpha). TNFR1 receptors were found on the majority of CGRP-containing rat trigeminal ganglion neurons. Treatment of cultures with TNF-alpha stimulated CGRP secretion. In addition, the intracellular signaling intermediate from the TNFR1 receptor, ceramide, caused a similar increase in CGRP release. TNF-alpha caused a coordinate increase in CGRP promoter activity. TNF-alpha treatment activated the transcription factor NF-kappaB, as well as the Jun N-terminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinase pathways. The importance of TNF-alpha induction of MAP kinase pathways was demonstrated by inhibiting MAP kinases with pharmacological reagents and gene transfer with an adenoviral vector encoding MAP kinase phosphatase-1 (MKP-1). We propose that selective and regulated inhibition of MAP kinases in trigeminal neurons may be therapeutically beneficial for inflammatory disorders involving elevated CGRP levels.
Mesh Headings (Keywords): Alzheimer Disease, Amino Acid Sequence, Amyloid beta-Protein, Animals, Basement Membrane, Biocompatible Materials, Blotting, Western, Cell Adhesion, Cell Survival, Collagen, Drug Combinations, Extracellular Matrix Proteins, Extracellular Signal-Regulated MAP Kinases, Laminin, Microscopy, Atomic Force, Molecular Sequence Data, Muscle, Smooth, Vascular, Peptide Fragments, Phosphorylation, Proteoglycans, Rats, Rats, Sprague-Dawley
Check for Full Text / PubMed Unique Identifier (PMID): 16277606
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