NMU

Official Full Name

neuromedin U

Organism

Homo sapiens

GeneID

10874

Background

This gene encodes a member of the neuromedin family of neuropeptides. The encoded protein is a precursor that is proteolytically processed to generate a biologically active neuropeptide that plays a role in pain, stress, immune-mediated inflammatory diseases and feeding regulation. Increased expression of this gene was observed in renal, pancreatic and lung cancers. Alternative splicing results in multiple transcript variants encoding different isoforms. Some of these isoforms may undergo similar processing to generate the mature peptide. [provided by RefSeq, Jul 2015]

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Detailed Information

Neuromedin U (NMU) is a neuropeptide isolated from porcine spinal cord in the 1980s, mainly NMU-25 and NMU-8. Its C-terminus has 7 amino acids identical to neuromedin S (NMS), so they bind a common receptor. NMU has two receptors (NMUR1 and NMUR2). NMU and its receptors are widely distributed in the nervous system and many tissues and organs, and have multiple biological functions, including stimulating smooth muscle contraction, regulating food intake and energy balance, affecting gastrointestinal function, reproductive endocrine, sleep and wakefulness.

NMU is widely distributed in the body, and there may be interspecific and developmental differences. In the central nervous system (CNS), the level of NMU in the spinal dorsal horn of the rat is higher than that of the ventral horn. In the brain, NMU immune activity (NMU-LIR) is found in the anterior motor nucleus, reticular nucleus, lateral vestibular nucleus, and trigeminal nucleus. NMU can contract smooth muscle but is species and tissue specific. Pigs' NMU-8 and NMU-25 shrink the uterus of rats, but not the uterine muscles of guinea pigs. NMU concentration-dependently mediates the small intestine contraction of turtles. NMU also mediates canine bladder, stomach, ileum, and colon contractions.

NMU Physiological Functions

NMU is involved in the regulation of food intake and energy balance. ICV injection of NMU in rats can reduce food intake and inhibit food-related behaviors. Intraventricular injection of NMU antiserum can increase food intake in rats, and fasting reduces NMU levels in the ventromedial region of the hypothalamus. The role of NMU in regulating feeding is mainly related to PVN and arcuate nucleus (Arc). Rats were injected with PVN or Arc NMU to immediately reduce food intake. Injecting NMU into the rat ventricle or PVN also increases total exercise activity, body temperature, heat production, and oxygen consumption. NMU injections also increased the body temperature of cattle. The mechanism by which the NMU regulates food intake and energy expenditure remains unclear. It may be related to oxytocin (OT), corticotropin-releasing hormone (CRF), leptin, and α-MSH. Intraventricular injection of CRF in rats inhibited food intake. Inhibition of food intake, oxygen consumption, and increase in body temperature observed after central administration of NMU were absent in CRF knockout mice.

NMU has a certain regulating effect on blood pressure and blood flow. Intravenous injection of NMU in rats can cause rapid and persistent arterial blood pressure rise. NMU increases heart rate, and high concentrations also increase plasma norepinephrine concentrations. These data indicate that NMU can increase sympathetic nerve activity. Intravenous NMU reduced blood flow to the anterior mesenteric artery and portal vein of anesthetized dogs, but had little or no effect on blood flow to the axillary and pancreatic tissues or systemic pulse pressure.

Figure 1. Summary of the multiple functions of NmU in different organs and tissue types. (Martinez, V. G. , et al. 2015)

Impact of NMU on Immunity

In LPS-treated NMU-deficient rats, IL-6 levels were significantly reduced. NMU and NMU-R1 are expressed in wild peritoneal macrophages. LMU treatment causes up-regulation of NMU expression, but down-regulates NMU-R1 expression. NMU-deficient macrophages showed no down-regulation of NMU-R1 expression, and LPS-induced IL-6 production was severely reduced. These results indicate that NMU promotes IL-6 and endotoxin shock in macrophages. Moriyama et al. found that the number of eosinophils in the airways of NMU-deficient mice induced by allergens was reduced. NMU-R1 is highly expressed in eosinophil cell lines. NMU directly induces Ca 2+ mobilization and extracellular/signal-regulated kinase phosphorylation, and also induces cell adhesion to extracellular matrix components (fibronectin and type I collagen) and chemotaxis in vitro. NMU-R1 is also expressed in human peripheral blood eosinophils, and NMU induces cell adhesion in a dose-dependent manner.

References:

Martinez, V. G. , & O'Driscoll, L. . (2015). Neuromedin u: a multifunctional neuropeptide with pleiotropic roles. Clinical Chemistry, 61(3), 471-482.
Cardoso, V. , Chesné, Julie, Ribeiro, Hélder, García-Cassani, Bethania, Carvalho, T. , & Bouchery, T. , et al. (2017). Neuronal regulation of type 2 innate lymphoid cells via neuromedin u. Nature.
Jowett, G. M. , & Neves, J. F. . (2018). Commentary: neuronal regulation of type 2 innate lymphoid cells via neuromedin u. Frontiers in Pharmacology, 9, 230-.

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