Spantide ([d-Arg1, d-Trp7,9, Leu11] substance P) was shown to function not only as a substance P receptor antagonist but also as a bombesin receptor antagonist. This study examined the effects of spantide on intravenous bombesin-induced stimulation of gastrin and acid secretion. Dogs were infused with spantide (1 or 10 nmol kg 1 hr 1) or saline and bombesin (60 pmol kg-1 hr-1), and the gastric acid and plasma gastrin responses were monitored. Spantide did not significantly modify gastrin or gastric acid secretion induced by bombesin. It is concluded that spantide may not be a useful bombesin antagonist for in vivo studies.
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http://dx.doi.org/10.1016/0196-9781(85)90335-3 | DOI Listing |
Clin Exp Pharmacol Physiol
July 2020
Department of Pharmacology, Kochi Medical School, Kochi University, Nankoku, Japan.
Excessive activation of the sympatho-adrenomedullary system plays a pathogenic role in triggering and sustaining essential hypertension. We previously reported that, in normotensive rats, intracerebroventricularly (i.c.
View Article and Find Full Text PDFBMC Cancer
November 2018
Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, E1354 BST, Pittsburgh, PA, 15261, USA.
Background: Head and neck squamous cell carcinoma (HNSCC) is the sixth leading cause of cancer death in the US. The protein kinase D (PKD) family has emerged as a promising target for cancer therapy with PKD1 being most intensively studied; however, its role in HNSCC has not been investigated.
Methods: The expression of PKD was evaluated in human HNSCC by quantitative RT-PCR, Western blot and immunohistochemistry.
J Biol Chem
June 2017
From the Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine,
Although PKC-mediated phosphorylation of protein kinase D1 (PKD1) has been extensively characterized, little is known about PKD1 regulation by other upstream kinases. Here we report that stimulation of epithelial or fibroblastic cells with G protein-coupled receptor agonists, including angiotensin II or bombesin, induced rapid and persistent PKD1 phosphorylation at Ser, a highly conserved residue located within the PKD1 N-terminal domain. Exposure to PKD or PKC family inhibitors did not prevent PKD1 phosphorylation at Ser, indicating that it is not mediated by autophosphorylation.
View Article and Find Full Text PDFAnticancer Res
November 2012
Department of Pediatric Surgery, 2200 Children's Way, DOT 7100, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Background: Intracellular signaling responsible for gastrin-releasing peptide (GRP) receptor-mediated neovascularization is not clearly understood. We sought to determine the cellular mechanisms involved in the GRP receptor regulation of vascular endothelial growth factor (VEGF) release in neuroblastoma cells.
Materials And Methods: BE(2)-C cells were treated with bombesin (BBS), the amphibian equivalent of GRP, Phorbol myristate acetate (PMA) a PKC agonist, or GF109293X (GFX), and analyses were performed for VEGF secretion, phosphorylated protein kinase B (AKT), extracellular signal-regulated kinases (ERK) and protein kinase D (PKD) expression.
Biol Pharm Bull
September 2008
Department of Applied Biological Science, Fukuyama University, Fukuyama, Japan.
Juniperonic acid (Delta-5c,11c,14c,17c-20:4, JA) is a polymethylene-interrupted (PMI) fatty acid that occurs in Biota orientalis. In this study, we found that JA has an antiproliferative activity. Swiss 3T3 cells were preloaded with fatty acids before stimulation with bombesin, a mitogenic neuropeptide, and proliferation of the cells was assessed by [(3)H]thymidine incorporation.
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