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| http://purl.uniprot.org/citations/27306412 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundVisceral hypersensitivity is a complex pathophysiological paradigm with unclear mechanisms. Primary afferent neuronal plasticity marked by alterations in neuroactive compounds such as calcitonin gene-related peptide is suggested to underlie the heightened sensory responses. Signal transduction that leads to calcitonin gene-related peptide expression thereby sensory neuroplasticity during colitis remains to be elucidated.ResultsIn a rat model with colitis induced by 2,4,6-trinitrobenzene sulfonic acid, we found that endogenously elevated brain-derived neurotrophic factor elicited an up-regulation of calcitonin gene-related peptide in the lumbar L1 dorsal root ganglia. At seven days of colitis, neutralization of brain-derived neurotrophic factor with a specific brain-derived neurotrophic factor antibody reversed calcitonin gene-related peptide up-regulation in the dorsal root ganglia. Colitis-induced calcitonin gene-related peptide transcription was also inhibited by brain-derived neurotrophic factor antibody treatment. Signal transduction studies with dorsal root ganglia explants showed that brain-derived neurotrophic factor-induced calcitonin generelated peptide expression was mediated by the phospholipase C gamma, but not the phosphatidylinositol 3-kinase/Akt or the mitogen-activated protein kinase/extracellular signal-regulated protein kinase pathway. Application of PLC inhibitor U73122 in vivo confirmed that colitis-induced and brain-derived neurotrophic factor-mediated calcitonin gene-related peptide up-regulation in the dorsal root ganglia was regulated by the phospholipase C gamma pathway. In contrast, suppression of the phosphatidylinositol 3-kinase activity in vivo had no effect on colitis-induced calcitonin gene-related peptide expression. During colitis, calcitonin gene-related peptide also co-expressed with phospholipase C gamma but not with p-Akt. Calcitonin gene-related peptide up-regulation during colitis correlated to the activation of cAMP-responsive element binding protein in the same neurons. Consistently, colitis-induced cAMP-responsive element binding protein activation in the dorsal root ganglia was attenuated by brain-derived neurotrophic factor antibody treatment.ConclusionThese results suggest that colitis-induced and brain-derived neurotrophic factor-mediated calcitonin generelated peptide expression in sensory activation is regulated by a unique pathway involving brain-derived neurotrophic factorphospholipase C gamma-cAMP-responsive element binding protein axis."xsd:string |
| http://purl.uniprot.org/citations/27306412 | http://purl.org/dc/terms/identifier | "doi:10.1177/1744806916657088"xsd:string |
| http://purl.uniprot.org/citations/27306412 | http://purl.uniprot.org/core/author | "Liu M."xsd:string |
| http://purl.uniprot.org/citations/27306412 | http://purl.uniprot.org/core/author | "Shen S."xsd:string |
| http://purl.uniprot.org/citations/27306412 | http://purl.uniprot.org/core/author | "Qiao L.Y."xsd:string |
| http://purl.uniprot.org/citations/27306412 | http://purl.uniprot.org/core/author | "Hashmi F."xsd:string |
| http://purl.uniprot.org/citations/27306412 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/27306412 | http://purl.uniprot.org/core/name | "Mol Pain"xsd:string |
| http://purl.uniprot.org/citations/27306412 | http://purl.uniprot.org/core/pages | "1744806916657088"xsd:string |
| http://purl.uniprot.org/citations/27306412 | http://purl.uniprot.org/core/title | "EXPRESS: Phospholipase C gamma mediates endogenous brain-derived neurotrophic factor - regulated calcitonin gene-related peptide expression in colitis - induced visceral pain."xsd:string |
| http://purl.uniprot.org/citations/27306412 | http://purl.uniprot.org/core/volume | "12"xsd:string |
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