Biochemical and Biophysical Research Communications
Regular ArticleB1 Bradykinin Receptors and Carboxypeptidase M Are Both Upregulated in the Aorta of Pigs after LPS Infusion☆,☆☆
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2016, TuberculosisCitation Excerpt :CPM activity, which plays an important role in BK production, is expressed on the plasma membrane of a broad variety of cells and tissues, including blood vessels, pneumocytes, macrophages and granulomas [24], preferentially induced in epithelioid cell (EPC) clusters of all granuloma types [40] and can be released from plasma membranes by bacterial phosphatidylinositol-specific phospholipase C activity [30]. Moreover, upregulation of CPM correlates to increasing endogenous levels of DABK and B1R agonists in bacterial lipopolysaccharide-induced inflammatory responses [29], while the DABK receptor B1R can be induced on cellular components of granulomas, including epithelial cells, macrophages, fibroblasts and lymphocytes [15,41,42]. Increased B1R but not B2R expression was found on macrophages at the center of granulomas in Crohn's disease [43], suggesting that DABK but not BK may play an important role in granuloma function.
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2013, Journal of Biological ChemistryCitation Excerpt :Thus, the CPM C-terminal domain containing residues 299–312 is involved in the allosteric interaction between B1R and CPM. CPM is present in human endothelial cells, and inflammatory cytokines can increase its expression 2–3-fold, conditions that also up-regulate B1R expression (6, 14, 31–33, 52). We thus used cytokine-treated HLMVEC to examine the allosteric effect of CPM on B1R function.
The arrestin-selective angiotensin AT<inf>1</inf> receptor agonist [Sar<sup>1</sup>,Ile<sup>4</sup>,Ile<sup>8</sup>]-AngII negatively regulates bradykinin B<inf>2</inf> receptor signaling via AT<inf>1</inf>-B<inf>2</inf> receptor heterodimers
2013, Journal of Biological ChemistryCitation Excerpt :B2 receptors are constitutively expressed in a majority of tissues and are particularly abundant in endothelium and VSMC (10). The B1 receptor is generally not expressed under physiological conditions but can be induced by inflammation, diabetes mellitus, and genetic deletion of the B2 receptor (11–13). B2 receptors couple to the Gq/11-phospholipase Cβ-PKC signaling pathway to promote calcium entry and to Gi/o proteins leading to inhibition of adenylyl cyclase-cAMP signaling (9).
Carboxypeptidase M
2013, Handbook of Proteolytic EnzymesThe kallikrein-kinin system in diabetic nephropathy
2012, Kidney InternationalCitation Excerpt :B2R is constitutively expressed in most tissues, including all segments of the kidney, and it mediates the majority of the physiological effects of kinins in health. In contrast, B1R is expressed at only low levels under physiological conditions, but its expression is induced by various pathological stimuli, such as ischemia/reperfusion injury,50 proinflammatory cytokines,51,52 diabetes,53 bacterial endotoxins,54 and angiotensin II,55 implying an important role of B1R activation under pathological situations. The cytokine-induced upregulation of B1R is mainly regulated by mitogen-activated protein kinase and nuclear factor-κB.51,56,57
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Abbreviations: LPS, lipopolysaccharide; BK, bradykinin.
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Farmer, S. G.
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Corresponding author. Fax: +49-89-5160-4486. E-mail: [email protected].