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- W2108798510 abstract "Stress affects immunity, but the mechanism is not known. Neurotensin (NT) and corticotropin-releasing hormone (CRH) are secreted under stress in various tissues, and have immunomodulatory actions. We had previously shown that NT augments the ability of CRH to increase mast cell-dependent skin vascular permeability in rodents. Here we show that NT triggered human mast cell degranulation and significantly augmented CRH-induced vascular endothelial growth factor (VEGF) release. Investigation of various signaling molecules indicated that only NF-κB activation was involved. These effects were blocked by pretreatment with the NTR antagonist SR48692. NT induced expression of CRH receptor-1 (CRHR-1), as shown by Western blot and FACS analysis. Interestingly, CRH also induced NTR gene and protein expression. These results indicate unique interactions among NT, CRH, and mast cells that may contribute to auto-immune and inflammatory diseases that worsen with stress." @default.
- W2108798510 created "2016-06-24" @default.
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- W2108798510 date "2012-11-14" @default.
- W2108798510 modified "2023-10-17" @default.
- W2108798510 title "Neurotensin and CRH Interactions Augment Human Mast Cell Activation" @default.
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- W2108798510 doi "https://doi.org/10.1371/journal.pone.0048934" @default.
- W2108798510 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3498358" @default.
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