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Neural Control of the Intestinal Circulation and its Interaction With Autoregulation
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Gerald A. Meininger, Harris J. Granger
Recently, very high levels of the peptide neuromedin U have been detected throughout the gastrointestinal tract (Domin et al., 1987; Augood et al., 1988). The highest levels of this peptide were found localized within the muscular layer of the small intestine (Domin et al., 1987; Augood et al., 1988) apparently in association with both the myenteric and submucosal nerve plexuses (Augood et al., 1988). Neuromedin U has also been reported to have the ability to significantly elevate blood pressure in rats (Minamino et al., 1985). When infused into dogs this peptide was found to be a potent and selective vasoconstrictor in the splanchnic circulation (Sumi et al., 1987). Collectively, these data suggest that neuromedin U may be a good candidate for further study as a neuropeptide involved in neural control of the intestinal circulation.
Gastroenteropancreatic Regulatory Peptide Structures: An Overview
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
Since McDonald’s last review of this topic approximately 5 years ago398 a number of novel peptides have been recognized, and it is probable that this process will continue. The endothelin story, which began just over 2 years ago, has developed with great rapidity and is the subject of a continuing intense investigation (vide supra). Minamino and colleagues399 isolated from porcine spinal cord two apparently novel pepties, designated neuromedin U or NMU. One peptide form was composed of 25 amino acid residues and contained the C-terminal Asn amide structure, and the second form, NMU18—25 was the C-terminal octa-peptide amide of the larger molecule. Rat NMU1—25 has also been isolated from the small intestine and the primary structure determined;400,401 there is a striking C-terminal structural conservation between rat and pig NMU, an area recognized as being of import for bioactivity. The significance of the tissue-specific distribution and the biological effects of neuromedin U are presently unknown, but are under investigation.402 In 1977, Price and Greenberg403 isolated a molluscan cardioexcitatory neuropeptide, the so-called FMRF-amide, which was named for its structure using the one-letter identifying codes for amino acids. FRMF-NH2 was demonstrated to have biological activity on administration to mammals, and immunologic evidence has been reported that a similar peptide exists in mammals. Recently Yang and colleagues404 isolated an octadecapeptide and an octapeptide from bovine brain which have C-terminal homology with each other and the same C-terminal dipeptide amide as the molluscan peptide. The physiological significance of these peptides and whether they are the mammalian equivalent to the molluscan FMRF-amide peptide are uncertain. The distribution of the mammalian peptides in the central nervous system has been described,405and the actions of FMRF-NH2 and related peptides in mammals have been reviewed recently.406 Schaller and Bodenmüller407 isolated a peptide from the coelenterate Hydra (designated the Hydra head activator) and determined its sequence to be Pyr–Pro–Pro–Gly–Gly–Ser–Lys–Val–Ile–Leu–Phe; recently, they have isolated an apparently identical peptide from rat intestine and human hypothalamus.408 The Hydra head activator peptide has been demonstrated to have bioactivity in mammals, but its physiological significance is unknown (for review see Reference 409 and citations therein). A recently isolated peptide, the monitor peptide, is composed of 61 amino acid residues and was first isolated from rat pancreatic juice; it possesses the capability of stimulating the release of cholecystokinin.410,411
Identification of vascular dementia and Alzheimer's disease hub genes expressed in the frontal lobe and temporal cortex by weighted co-expression network analysis and construction of a protein–protein interaction
Published in International Journal of Neuroscience, 2022
Xiaodou Tian, Yao Qin, Yuling Tian, Xiaoyan Ge, Jing Cui, Hongjuan Han, Long Liu, Hongmei Yu
There were three hub genes in the VaD group. The neuropeptide neuromedin U (NMU), which binds to its corresponding neuropeptide receptor; the neuropeptide somatostatin (SST), which binds to G protein coupled receptors; TAC1 encoding the ligand substance P (SP), which affects vasoconstriction and relaxation. According to our PPI network the above genes might jointly interact to cause VaD and their relevance were similar (Figure 6(a)). VaD would be involved in the increase of vascular permeability, the promotion of neuroinflammatory response and eventually led to the death of nerve cells.
Role of eosinophils in protective immunity against secondary nematode infections
Published in Immunological Medicine, 2019
The function of eosinophils as a defense against parasites is well-known; however, eosinophils have been reported to have additional roles in allergic inflammation and tissue repair, as well as immunomodulation [42–44]. Regarding the eosinophil-mediated mechanism of defense against parasites, binding to the worm larvae through antibody or complement, followed by release of intracellular granules, is presumed to cause injury to invading worms [45–49]. The numbers of eosinophils increase with helminth infection. Löffler found a link between parasite infection and pulmonary eosinophilia (Löffler’s syndrome) [50]. Although the mechanism underlying this eosinophil accumulation has been unknown for many years, we elucidated the mechanism using a Strongyloides venezuelensis infection model [38]. Some parasitic enteric nematode larvae, including S. venezuelensis and N. brasiliensis, do not migrate directly to the gut upon percutaneous or oral infection. Instead, they migrate to the lungs via the bloodstream, then penetrate the alveolar cavity and travel to the throat, where they are swallowed. Finally, they reach the small intestine and mature [51,52]. As the larvae pass through the lungs, they cause damage to lung tissue, stimulating the release of IL-33 from type II alveolar epithelial cells. IL-33-deficient mice showed a marked reduction in eosinophil accumulation upon S. venezuelensis infection. Conversely, nasal administration of IL-33 can induce pulmonary eosinophilia even in Rag2-deficient mice that lack both T cells and B cells [38]. IL-33 stimulates ILC2s to proliferate and accumulate in the lungs, and induces production of IL-5 and IL-13 by ILC2s. Excretory/secretory products from N. brasiliensis stimulate neuronal production of neuromedin U, which stimulates ILC2s to produce Th2 cytokines. These combined actions result in the onset of lung eosinophilic inflammation [53].
Autism spectrum disorders and natural killer cells: a review on pathogenesis and treatment
Published in Expert Review of Clinical Immunology, 2021
Sepideh Ebrahimi Meimand, Yasna Rostam-Abadi, Nima Rezaei
Neuromedin U Receptor 1 (NMUR1) is a protein-encoding gene and its transcription occurs in T cells and NK cells [96]. The protein binds to Neuromedin U which is a multifunctional neuropeptide. It has roles in inflammation and secretion of cytokines [97]. Down-regulation of NMUR1 in children with ASD suggests the reduced cytotoxicity of NK cells in them.