Disease relevance of Grp-10

• In contrast, L-364,718 administered at identical dosages, did not affect pancreatic hypertrophy induced by bombesin and neuromedin C [1].
• 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 nmol/rat) did not significantly inhibit the neuromedin C-induced hyperalgesia [2].
• The findings indicated that NMC caused moderate hypothermia following intracerebroventricular administration, while the effect of NMB was meager, suggesting that these two neuropeptides possess different physiological functions in the brain [3].

Psychiatry related information on Grp-10

• Intrathecal injection of bombesin and neuromedin C to the lower lumbar vertebral level produced a dose-dependent decrease in reaction time which lasted up to 46 min [4].

High impact information on Grp-10

• RESULTS: Interleukin (IL) 1 beta (50% effective concentration [EC50], 5.3 +/- 0.4 ng/mL) and tumor necrosis factor (TNF) alpha (EC50, 5.5 +/- 0.5 ng/mL) stimulated gastrin release to 50% of the maximal response to 10(-9) mol/L neuromedin C [5].
• Stimulation by IL-1 beta and TNF-alpha was additive to the responses to neuromedin C and O2-dibutyryl adenosine 3',5'-cyclic monophosphate [5].
• Isolation of endopeptidase-24.11 (EC 3.4.24.11, "enkephalinase") from the pig stomach. Hydrolysis of substance P, gastrin-releasing peptide 10, [Leu5] enkephalin, and [Met5] enkephalin [6].
• Neuromedin C had almost the same bioactivity as GRP with respect to the release of PP, whereas neuromedin B was one-third less potent than GRP and neuromedin C [7].
• Relative binding affinity of GRP analogues was in the order of GRP (14-27) greater than neuromedin C greater than or equal to BBS greater than or equal to GRP (1-27) greater than neuromedin B (for the later, P greater than 0.05 versus other peptides) [8].

Biological context of Grp-10

• These results suggest that inositol phospholipid signalling and cAMP messenger systems are involved in the increase of NK and ADCC activities when leukocytes are incubated in the presence of bombesin, GRP or neuromedin C [9].
• Immunoreactive neuromedin B and neuromedin C were characterized and measured in rat and human tissue extracts, using radioimmunoassay combined with gel filtration and high performance liquid chromatography in order to clarify tissue distribution and molecular structure [10].
• By microsequencing and synthesis, the amino acid sequence of the peptide has been identified as: Gly-Asn-His-Trp-Ala-Val-Gly-His-Leu-Met-NH2 [11].
• Our results indicate that gastrin-releasing peptide-10 and neuromedin B delay gastric emptying by acting on distinct receptors in rats, in vivo [12].
• Gastrin-releasing peptide (GRP) and neuromedin C caused a higher activation of adherence, chemotaxis and ingestion of C. albicans than bombesin [13].

Anatomical context of Grp-10

• Extracts of guinea pig brain and small intestine contained both gastrin-releasing peptide and its COOH-terminal decapeptide (neuromedin C) but the stomach extracts contained only gastrin-releasing peptide [14].
• Stimulation of natural killer and antibody-dependent cellular cytotoxicity activities in mouse leukocytes by bombesin, gastrin-releasing peptide and neuromedin C: involvement of cyclic AMP, inositol 1,4,5-trisphosphate and protein kinase C [9].
• The neuropeptide, neuromedin C, activates a potassium current in mouse macrophages [15].
• This was examined using the isolated perfused porcine ileum stimulated with acetylcholine (ACh, 10(-6) M), neuromedin C (NC, 10(-8) M), and electrical nerve stimulation (NS) with or without alpha-adrenergic blockade (phentolamine 10(-5) M), and perfusion with a high-affinity monoclonal antibody against SS [16].
• The primed oocytes responded to peptides of the bombesin family (GRP, neuromedin C of bombesin) by showing dose-dependent oscillations in membrane currents as recorded by the voltage-clamp method [17].

Associations of Grp-10 with other chemical compounds

• These potencies differed from those for the GRP receptor subtype on rat pancreatic acini [Bn approximately equal to litorin (4 nM) greater than ranatensin, NMC, GRP (15-20 nM) much greater than NMB (351 nM)] [18].
• The actions of the peptides bombesin (BN), gastrin releasing peptide (GRP), neuromedin C (NMC), litorin and neuromedin B (NMB) were studied on neurons in slices of rat brain maintained in vitro to determine the BN receptor type present in different brain areas [19].
• The neuropeptide function of neuromedin C and/or other BLI peptides at this level was supported by the stimulatory effect of carbamylcholine (500 microM) on the release of BLI (4.5-fold increase over the basal release of 19 fmol/5 min) from perfused bovine adrenal glands [20].
• Perifusion of rat anterior pituitary cell aggregates, cultured in estrogen-supplemented serum-free medium with 1 nM of the bombesin (BBN)-like peptide, neuromedin C (NMC), significantly stimulates GH and PRL release [21].
• All bombesin-like peptides in pmol ranges exhibited potent stimulatory effects on the firing of arcuate neurons, i.e., gastrin-releasing peptide stimulated 90.9% (n = 22), bombesin 78.0% (n = 41), neuromedin C 63.2% (n = 19), ranatensin 58.0% (n = 22), and neuromedin B 50.0% (n = 6) of arcuate neurons tested [22].

Gene context of Grp-10

• The number of HT-29 cells, partially serum deprived (1% fetal bovine serum) for 48 h, was increased after 24 h of stimulation with bombesin, GRP, neuromedin B (NMB) and neuromedin C (NMC) ranging from 0.1 nM up to 1 microM [23].
• Bombesin (EC50 6 X 10(-11) M), its mammalian analog GRP-27, and neuromedin C (GRP-10) (EC50 1 X 10(-10) M, for both) were almost equally potent stimuli of somatostatin release, eliciting maximal response at 10(-9) M (400-550% above basal) [24].
• Comparison of the actions of bombesin, gastrin-releasing peptide-27, neuromedin B, and gastrin-releasing peptide-10 in causing release of gastrin and gastric inhibitory peptide in rats [25].
• The CCKB/gastrin receptor antagonist CI-988 (1 microM) had no effect on either GRP- or NMC-mediated excitation [19].
• Bombesin-related peptides which include bombesin, neuromedin B, and neuromedin C induced significant [Ca2+]i transients in RPE cells, whereas other neuropeptides, neuropeptide Y, vasoactive intestinal polypeptide (VIP), and substance P were not effective to produce [Ca2+]i transients [26].

Analytical, diagnostic and therapeutic context of Grp-10

• There was no significant difference between the levels of immunoreactivity in 12-h light and 12-h dark adapted retinae. rp HPLC analysis of retinal extracts demonstrated that two main immunoreactive components were present which corresponded in retention time to GRP10 (neuromedin C) and GRP14 (GRP14-27) [27].
• The CCK release produced by intra-arterial infusion of neuromedin C was inhibited by EABI in a dose-dependent manner [28].
• Extracts of rat brain and gastrointestinal tract, analyzed by reverse-phase high-performance liquid chromatography and radioimmunoassay, contained two bombesin-like immunoreactivity peaks with similar retention times as porcine gastrin-releasing peptide (GRP) and its COOH-terminal decapeptide, neuromedin C or GRP(18-27) [29].
• However, responses to intravenous injection of neuromedin C, to intraduodenal injection of capsaicin, and to intragastric injection of a liquid meal were impaired in OLETF rats [30].
• Intravenous infusion of CR-1409, a specific CCK-receptor antagonist, inhibited, but did not abolish, the protein secretion stimulated by neuromedin C [31].

References