Bradykinin prevents the apoptosis of NIT-1 cells induced by TNF-α via the PI3K/Akt and MAPK signaling pathways

Xu, Xizhen; Tu, Lei; Jiang, Wei; Feng, Wenjing; Zhao, Chun‐Xia; Wang, Dao Wen

doi:10.3892/ijmm.2012.922

Cited by 16 publications

(13 citation statements)

References 25 publications

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“…KKS is a complex multi-enzyme system composed of circulating and tissue kallikrein and kinin. It is well established that tissue kallikrein and kinin play crucial and diverse roles in cardiovascular and renal homeostasis [10]. Our previous data also show that kallikrein gene delivery reduces blood pressure and ameliorates renal function in spontaneously hypertensive and 5/6 nephrectomized rats [11].…”

Section: Introductionmentioning

confidence: 52%

Bradykinin Inhibits Oxidative Stress-Induced Cardiomyocytes Senescence via Regulating Redox State

Dong

et al. 2013

PLoS ONE

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BackgroundCell senescence is central to a large body of age related pathology, and accordingly, cardiomyocytes senescence is involved in many age related cardiovascular diseases. In consideration of that, delaying cardiomyocytes senescence is of great importance to control clinical cardiovascular diseases. Previous study indicated that bradykinin (BK) protected endothelial cells from senescence induced by oxidative stress. However, the effects of bradykinin on cardiomyocytes senescence remain to be elucidated. In this study, we investigated the effect of bradykinin on H2O2-induced H9C2 cells senescence.Methods and ResultsBradykinin pretreatment decreased the senescence induced by H2O2 in cultured H9C2 cells in a dose dependent manner. Interestingly, 1 nmol/L of BK almost completely inhibited the increase in senescent cell number and p21 expression induced by H2O2. Since H2O2 induces senescence through superoxide-induced DNA damage, we also observed the DNA damage by comet assay, and BK markedly reduced DNA damage induced by H2O2, and moreover, BK treatment significantly prevented reactive oxygen species (ROS) production in H9C2 cells treated with H2O2. Importantly, when co-incubated with bradykinin B2 receptor antagonist HOE-140 or eNOS inhibitor N-methyl-L-arginine acetate salt (L-NAME), the protective effects of bradykinin on H9C2 senescence were totally blocked. Furthermore, BK administration significantly prevented the increase in nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity characterized by increased ROS generation and gp91 expression and increased translocation of p47 and p67 to the membrane and the decrease in superoxide dismutase (SOD) activity and expression induced by H2O2 in H9C2 cells, which was dependent on BK B2 receptor mediated nitric oxide (NO) release.ConclusionsBradykinin, acting through BK B2 receptor induced NO release, upregulated antioxidant Cu/Zn-SOD and Mn-SOD activity and expression while downregulating NADPH oxidase activity and subsequently inhibited ROS production, and finally protected against cardiomyocytes senescence induced by oxidative stress.

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Section: Introductionmentioning

confidence: 52%

Bradykinin Inhibits Oxidative Stress-Induced Cardiomyocytes Senescence via Regulating Redox State

Dong

et al. 2013

PLoS ONE

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“…PI3K-dependent Akt activation has been shown to play an important role in BK-mediated cellular functions [26,27,39]. We demonstrated that treatment with a PI3K inhibitor and Akt inhibitor inhibited BK-induced cell motility and ICAM-1 expression, suggesting that PI3K/Akt activation is a requisite event in BK-increased cell migration in prostate cancer cells.…”

Section: Discussionmentioning

confidence: 61%

“…PI3K/Akt activation has been reported to occur in BK-mediated cell functions [26,27]. To examine whether PI3K is involved in BK-induced cell migration, the PI3K inhibitor Ly294002 was used.…”

Section: Resultsmentioning

confidence: 99%

Involvement of Intercellular Adhesion Molecule-1 Up-Regulation in Bradykinin Promotes Cell Motility in Human Prostate Cancers

Lin

Tang

2013

IJMS

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Prostate cancer is the most commonly diagnosed malignancy in men and shows a predilection for metastasis to distant organs. Bradykinin (BK) is an inflammatory mediator and has recently been shown to mediate tumor growth and metastasis. The adhesion molecule intercellular adhesion molecule-1 (ICAM-1) plays a critical role during tumor metastasis. The aim of this study was to examine whether BK promotes prostate cancer cell migration via ICAM-1 expression. The motility of cancer cells was increased following BK treatment. Stimulation of prostate cancer cells with BK induced mRNA and protein expression of ICAM-1. Transfection of cells with ICAM-1 small interfering RNA reduced BK-increased cell migration. Pretreatment of prostate cancer cells with B2 receptor, phosphatidylinositol 3-kinase (PI3K), Akt, and activator protein 1 (AP-1) inhibitors or mutants abolished BK-promoted migration and ICAM-1 expression. In addition, treatment with a B2 receptor, PI3K, or Akt inhibitor also reduced BK-mediated AP-1 activation. Our results indicate that BK enhances the migration of prostate cancer cells by increasing ICAM-1 expression through a signal transduction pathway that involves the B2 receptor, PI3K, Akt, and AP-1. Thus, BK represents a promising new target for treating prostate cancer metastasis.

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“…This seems to corroborate the findings reported so far in animal models 33,34 as well as experimental studies on degenerative disease and cell aging processes in humans. 24,25,[35][36][37][38][39] Our results concerning oxidative stress in C1--INH -HAE as well as the effect of bradykinin on oxidative stress in PBMCs in this patient population were presented as preliminary findings during 2018 Bradykinin Symposium in Berlin. 40 They are generally consistent with the recent study by Del Giacco et al, 18 who indicated Our results concerning the effect of exogenous bradykinin on basal and H 2 O 2 -induced ROS levels in PBMCs in patients with C1 -INH -HAE showed that bradykinin exerted a significant antioxidant effect in this group of patients.…”

Section: What's New?mentioning

confidence: 83%

Bradykinin and oxidative stress in patients with hereditary angioedema due to C1 inhibitor deficiency

Obtułowicz¹,

Góralska²,

Bogdali-Suślik³

et al. 2020

Polish Archives of Internal Medicine

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INTROduCTION Hereditary angioedema (HAE) is a rare autosomal dominant disease caused by genetic dysfunction of C1 inhibitor (C1-INH) due to mutations in the SERPING1 gene. The disorder is mediated mainly by bradykinin. The clinical course of the disease is varied and not related to genetic changes. OBjECTIvEs We aimed to evaluate redox homeostasis of peripheral blood mononuclear cells (PBMCs) in patients with HAE due to C1-INH deficiency (C1-INH-HAE) by measuring the levels of reactive oxygen species (ROS) of PBMCs as well as plasma advanced glycation end products (AGEs) and advanced oxidation protein products (AOPPs). We also aimed to assess the effect of bradykinin on ROS levels. PATIENTs ANd mEThOds We enrolled 30 adults with C1-INH-HAE and 15 healthy individuals. The levels of ROS were measured by flow cytometry, while the plasma levels of AGEs and AOPPs were determined spectrophotometrically by enzyme-linked immunosorbent assays. REsuLTs Basal and hydrogen peroxide (H 2 O 2)-induced ROS levels were higher in patients with HAE when compared with controls (P = 0.002 and P = 0.001, respectively), indicating abnormalities in redox homeostasis. Plasma AOPP and AGE levels were similar in both groups. Bradykinin reduced basal and H 2 O 2-induced ROS generation in PBMCs only in patients with HAE (P = 0.03). CONCLusIONs The higher basal and H 2 O 2-induced ROS levels in patients with C1-INH-HAE indicate redox imbalance. However, by reducing basal and H 2 O 2-induced ROS levels, bradykinin shows antioxidant action in this disorder.

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Bradykinin prevents the apoptosis of NIT-1 cells induced by TNF-α via the PI3K/Akt and MAPK signaling pathways

Cited by 16 publications

References 25 publications

Bradykinin Inhibits Oxidative Stress-Induced Cardiomyocytes Senescence via Regulating Redox State

Bradykinin Inhibits Oxidative Stress-Induced Cardiomyocytes Senescence via Regulating Redox State

Involvement of Intercellular Adhesion Molecule-1 Up-Regulation in Bradykinin Promotes Cell Motility in Human Prostate Cancers

Bradykinin and oxidative stress in patients with hereditary angioedema due to C1 inhibitor deficiency

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