Participation of kallikrein–kinin system in different pathologies

Costa-Neto, Cláudio M.; Dillenburg-Pilla, Patrícia; Heinrich, Tassiele A.; Parreiras-e-Silva, Lucas T.; Pereira, Marilia G.A.G.; Reis, Rosana I.; Souza, Pedro Paulo Chaves de

doi:10.1016/j.intimp.2007.08.003

Cited by 76 publications

(52 citation statements)

References 118 publications

(120 reference statements)

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“…Bradykinin (BK) and kallidin (Lys-BK), collectively called the kinins, are potent bioactive peptides which ubiquitously occur in body fl uids and tissues and play regulatory roles in numerous physiological as well as pathological processes (Bhoola, Figueroa, & Worthy, 1992;Blais, Marceau, Rouleau, & Adam, 2000;Joseph & Kaplan, 2005;Costa-Neto et al, 2008). BK belongs to the major regulators of arterial blood pressure.…”

Section: Introductionmentioning

confidence: 99%

Bradykinin and des-Arg¹⁰-kallidin enhance the adhesion of polymorphonuclear leukocytes to extracellular matrix proteins and endothelial cells

Guevara-Lora

Łabędź

Skrzeczyńska‐Moncznik

et al. 2011

Cell Communication & Adhesion

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Bradykinin-related peptides (kinins) are well known to contribute to leukocyte recruitment to infl ammatory foci; however, a role of these universal pro-infl ammatory mediators in the fi rst step of this process, i.e. the leukocyte adhesion to endothelial cells, is not well understood. In this work we found that bradykinin and des-Arg 10 -kallidin enhance the adhesion of polymorphonuclear bloods cells (PMN) to fi brinogen and fi bronectin. Also, the PMN adherence to endothelial cells of HMEC-1 line strongly increased after stimulation by kinins, particularly des-Arg 10 -kallidin, or when PMN were costimulated with bradykinin and interleukin-1 β . These effects were attenuated after PMN treatment with a specifi c inhibitor of carboxypeptidases, which convert kinins to their des-Arg metabolites. The kinin peptides were also able to change the Mac-1 integrin expression on the PMN surface. These results suggest a regulatory effect of kinins on leukocyte adhesion to endothelial wall, providing new aspects of the leukocyte infi ltration into infl amed tissues.

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Section: Introductionmentioning

confidence: 99%

Bradykinin and des-Arg¹⁰-kallidin enhance the adhesion of polymorphonuclear leukocytes to extracellular matrix proteins and endothelial cells

Guevara-Lora

Łabędź

Skrzeczyńska‐Moncznik

et al. 2011

Cell Communication & Adhesion

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“…Frey and coworkers; they extracted it from snake venom (Costa-Neto et al, 2008). The KKS consists of precursor kininogens, kallikrein and the kinin peptides.…”

Section: Kallikrein-kinin System (Kks) Was Discovered In 1928 Bymentioning

confidence: 99%

The Roles of Cycloxygenase and Endothelial Derived Hyperpolarizing Factors in Bradykinin-Induced Aortic Relaxation

Omar¹,

Maulood²

2017

SJUOZ

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ABSTRACT:The present study is designed to investigate the roles of cycloxygenase (COX) and endothelial derived hyperpolarizing factors (EDHF) pathways in bradykinin (BK)-induced aortic relaxation. Here, isolated aortic rings pre-incubated with different ion channel blockers which are; inward rectifier potassium channel blocker (barium chloride; BaCl2), calcium activated Potassium (KCa+2) channel blocker (tetraethylammonium; TEA), cytochrome P450 inhibitor, clotrimazole and cycloxygenase inhibitor and indomethacin. In BaCl2, Emax tended to decrease significantly with significant change of PIC50. TEA pre-incubation markedly shifted DRC of BK to the left side and it significantly reduced PIC50. Indomethacin significantly lowered the PIC50 of BK, but it shifted the DRC of BK to the left. The results suggested that BK relaxes aortic smooth muscle particularly via the enhancement of cycloxygenase and epoxygenase enzymes as well as through opening Kir and KCa +2 channels.

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“…The kallikrein-kinin system (KKS) is a complex multi-enzyme system that is widespread across various tissues and shows a variety of biological activities (Wright et al, 2008;Costa-Neto et al, 2008;Tang et al, 2011;Phipps et al, 2012). Recent studies have found that the KKS could significantly inhibit glomerulosclerosis (Schanstra et al, 2002;Marceau and Regoli, 2004;Kakoki et al, 2004;Tan et al, 2005;Tomita et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Effect of bradykinin on renal mesangial cell proliferation and extracellular matrix secretion

Liu¹,

Zhou²,

Cheng³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Recent studies have found that bradykinin (BK) plays a role in delaying glomerulosclerosis, although the mechanism of this phenomenon remains unclear. Mesangial cell proliferation (MCP) and extracellular matrix (ECM) secretion are important mechanisms for glomerulosclerosis. This study investigated the impact of BK on the platelet-derived growth factor (PDGF)-induced proliferation of mesangial cells, and evaluated its correlations with the extracellular signal-related kinase (ERK) signaling pathway. The results showed that on its own, 10-1000 mg/L BK promoted MCP and ECM secretion and induced ERK phosphorylation. However, BK administration after PDGF pre-incubation inhibited PDGF-induced MCP, ECM secretion, and ERK phosphorylation. The BK B2 receptor-specific antagonist, HOE-140, and tyrosine phosphatase inhibitor (OV) effectively blocked the function of BK. In summary, these results demonstrated that BK has a bidirectional effect on MCP and ECM secretion: when used alone, it promoted effects on these phenomena, but these effects were inhibited when combined with PDGF. This suggests that the role of BK might be achieved through inhibiting activation of the PDGF-induced ERK1/2 pathway.

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Participation of kallikrein–kinin system in different pathologies

Cited by 76 publications

References 118 publications

Bradykinin and des-Arg¹⁰-kallidin enhance the adhesion of polymorphonuclear leukocytes to extracellular matrix proteins and endothelial cells

Bradykinin and des-Arg¹⁰-kallidin enhance the adhesion of polymorphonuclear leukocytes to extracellular matrix proteins and endothelial cells

The Roles of Cycloxygenase and Endothelial Derived Hyperpolarizing Factors in Bradykinin-Induced Aortic Relaxation

Effect of bradykinin on renal mesangial cell proliferation and extracellular matrix secretion

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Participation of kallikrein–kinin system in different pathologies

Cited by 76 publications

References 118 publications

Bradykinin and des-Arg10-kallidin enhance the adhesion of polymorphonuclear leukocytes to extracellular matrix proteins and endothelial cells

Bradykinin and des-Arg10-kallidin enhance the adhesion of polymorphonuclear leukocytes to extracellular matrix proteins and endothelial cells

The Roles of Cycloxygenase and Endothelial Derived Hyperpolarizing Factors in Bradykinin-Induced Aortic Relaxation

Effect of bradykinin on renal mesangial cell proliferation and extracellular matrix secretion

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Bradykinin and des-Arg¹⁰-kallidin enhance the adhesion of polymorphonuclear leukocytes to extracellular matrix proteins and endothelial cells

Bradykinin and des-Arg¹⁰-kallidin enhance the adhesion of polymorphonuclear leukocytes to extracellular matrix proteins and endothelial cells