Is the expression of kinin B1 receptor related to intrahepatic vascular response?

Nagaoka, Márcia Regina; Gomiero, Luciana; Teixeira, Felipe de Oliveira; Agostino, Fernando G.; Pouza, José Eduardo P.; Mimary, Priscila; Borges, Durval Rosa; Kouyoumdjian, Maria

doi:10.1016/j.bbagen.2006.08.009

Cited by 7 publications

(5 citation statements)

References 23 publications

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“…Kinin B1R is an important inflammatory mediator and is correlated to the hemodynamic response to kinins, with increased blood pressure induced by des-Arg 9 -bradykinin [42, 43]. In hepatic perfusion, BK induces a portal hypertensive response that is mediated by B2R and modulated by NO system in healthy liver, as well as, in inflammatory, fibrotic, and cirrhotic conditions [28].…”

Section: Discussionmentioning

confidence: 99%

Malaria infection promotes a selective expression of kinin receptors in murine liver

Ventura

Carvalho

Barros

et al. 2019

Malar J

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Background Malaria represents a worldwide medical emergency affecting mainly poor areas. Plasmodium parasites during blood stages can release kinins to the extracellular space after internalization of host kininogen inside erythrocytes and these released peptides could represent an important mechanism in liver pathophysiology by activation of calcium signaling pathway in endothelial cells of vertebrate host. Receptors (B1 and B2) activated by kinins peptides are important elements for the control of haemodynamics in liver and its physiology. The aim of this study was to identify changes in the liver host responses (i.e. kinin receptors expression and localization) and the effect of ACE inhibition during malaria infection using a murine model. Methods Balb/C mice infected by Plasmodium chabaudi were treated with captopril, an angiotensin I-converting enzyme (ACE) inhibitor, used alone or in association with the anti-malarial chloroquine in order to study the effect of ACE inhibition on mice survival and the activation of liver responses involving B1R and B2R signaling pathways. The kinin receptors (B1R and B2R) expression and localization was analysed in liver by western blotting and immunolocalization in different conditions. Results It was verified that captopril treatment caused host death during the peak of malaria infection (parasitaemia about 45%). B1R expression was stimulated in endothelial cells of sinusoids and other blood vessels of mice liver infected by P. chabaudi . At the same time, it was also demonstrated that B1R knockout mice infected presented a significant reduction of survival. However, the infection did not alter the B2R levels and localization in liver blood vessels. Conclusions Thus, it was observed through in vivo studies that the vasodilation induced by plasma ACE inhibition increases mice mortality during P. chabaudi infection. Besides, it was also seen that the anti-malarial chloroquine causes changes in B1R expression in liver, even after days of parasite clearance. The differential expression of B1R and B2R in liver during malaria infection may have an important role in the disease pathophysiology and represents an issue for clinical treatments.

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Section: Discussionmentioning

confidence: 99%

Malaria infection promotes a selective expression of kinin receptors in murine liver

Ventura

Carvalho

Barros

et al. 2019

Malar J

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“…Overexpression of endothelial bradykinin B1 receptors occurs in livers of rats with experimental cirrhosis (23). Endothelial bradykinin B1 receptors bind to des-Arg1-BK, which promotes inflammation.…”

Section: Sars-cov-2 and The Non-classical Rasmentioning

confidence: 99%

Pathways of hepatic and renal damage through non‐classical activation of the renin‐angiotensin system in chronic liver disease

Sansoè

Aragno

2019

Liver International

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List of abbreviations. ACE, angiotensin converting enzyme. ACE2, angiotensin converting enzyme type 2. ACEi, angiotensin converting enzyme inhibitor. ADAM-17, a disintegrin and metalloproteinase domain-17. ALT, alanine aminotransferase. Ang II, angiotensin II. Ang1-7, angiotensin 1-7. ARB, angiotensin type 1 receptor antagonist. ARDS, acute respiratory distress syndrome. AST, aspartate aminotransferase. AT1R, angiotensin type 1 receptor. AT2R, angiotensin type 2 receptor. BDL, bile duct ligation. des-Arg1-BK, des-arginine bradykinin. ERK, extracellular signal-regulated kinase. HCC, hepatocellular carcinoma. IL, interleukin. MasR, Mas receptor. MRGD, Mas-related G protein-coupled receptor member D. NAFLD, non-alcoholic fatty liver disease. NEP, neprilysin. RAS, renin-angiotensin system. sACE2, soluble ACE2. SARS, severe acute respiratory syndrome. SARS-CoV-2, severe acute respiratory syndrome coronavirus 2. TNFα, tumor necrosis factor-α.

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“…B1Rs are induced by stimulation of lipopolysaccharides, IL-1β and TNFα, by tissue injury and exposure to kinins (the receptor agonists) via activation of NF-ĸB signaling pathway [6,7,[15][16][17][18]25]. B1 receptor induction elicits persistent inflammatory responses and its up-regulation is further boosted by ligand binding [17,26]. Therefore, kinin B1 receptors may be important in maintaining chronic inflammatory processes, such as chronic liver injury [8].…”

Section: B1rs In Hepatic Inflammationmentioning

confidence: 99%

Kinin B1 receptor blockade attenuates hepatic fibrosis and portal hypertension in chronic liver diseases in mice

et al. 2022

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Background and aims Kinin B1 receptors (B1Rs) are implicated in the pathogenesis of fibrosis. This study examined the anti-fibrotic effects of B1R blockade with BI 113823 in two established mouse models of hepatic fibrosis induced by intraperitoneal carbon tetrachloride (CCl4) injection or bile duct ligation (BDL). The mechanisms underlying the protection afforded by B1R inhibition were examined using human peripheral blood cells and LX2 human hepatic stellate cells (HSCs). Methods Fibrotic liver diseases were induced in mice by intraperitoneal carbon tetrachloride (CCl4) injection for 6 weeks, and by bile duct ligation (BDL) for 3 weeks, respectively. Mice received daily treatment of vehicle or BI 113823 (B1R antagonist) from onset of the experiment until the end of the study. Results B1Rs were strongly induced in fibrotic mouse liver. BI 113823 significantly attenuated liver fibrosis and portal hypertension (PH), and improved survival in both CCl4 and BDL mice. BI 113823 significantly reduced the expression of fibrotic proteins α-SMA, collagens 1, 3, 4, and profibrotic growth factors PDGF, TGFβ, CTGF, VEGF, proliferating cell nuclear antigen; and reduced hepatic Akt phosphorylation in CCl4- and BDL-induced liver fibrosis. BI 113823 also reduced expression of Cytokines IL-1, IL-6; chemokines MCP-1, MCP-3 and infiltration of inflammatory cells; and inhibited human monocyte and neutrophil activation, transmigration, TNF-α & MPO production in vitro. BI 113823 inhibited TGF-β and B1R agonist-stimulated human-HSC activation, contraction, proliferation, migration and fibrosis protein expression, and inhibited activation of PI3K/Akt signalling pathway. Conclusions B1Rs merits consideration as a novel therapeutic target for chronic liver fibrosis and PH.

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Is the expression of kinin B1 receptor related to intrahepatic vascular response?

Cited by 7 publications

References 23 publications

Malaria infection promotes a selective expression of kinin receptors in murine liver

Malaria infection promotes a selective expression of kinin receptors in murine liver

Pathways of hepatic and renal damage through non‐classical activation of the renin‐angiotensin system in chronic liver disease

Kinin B1 receptor blockade attenuates hepatic fibrosis and portal hypertension in chronic liver diseases in mice

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