Nitric oxide and superoxide in rat mesangial cells: modulation by C-reactive protein

Trachtman, Howard; Futterweit, Stephen; Arzberger, Christopher; Bod, Jessica; Goldschmiedt, Judah; Gorman, Haddassah; Reddy, Krishna; Franki, Nicholas; Singhal, Pravin C.

doi:10.1007/s00467-006-0066-x

Cited by 11 publications

(7 citation statements)

References 44 publications

(57 reference statements)

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“…Prasad [32] have shown that in neutrophils, CRP significantly and dose-dependently induces superoxide anion release in vitro, however, no mechanistic studies were undertaken. Exposure of rat mesangial cells to CRP for 60 min led to a dose-dependent increase in superoxide anion release that was nearly threefold greater than that in the control conditions (p < 0.0001) [33]. They also showed that co-incubation with DPI (10 μM) prevented the increase in superoxide production by rat mesangial cells induced by CRP (100 μg/mL).…”

Section: Discussionmentioning

confidence: 90%

C-reactive protein stimulates superoxide anion release and tissue factor activity in vivo

et al. 2009

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C-reactive protein (CRP), the prototypic marker of inflammation, is a cardiovascular risk marker and recent in vitro studies suggest that it may promote atherogenesis. CRP promotes oxidative stress in vitro and induces tissue factor (TF) release. However, there is a paucity of data examining the effects of CRP on oxidative stress and tissue factor procoagulant activity (PCA) in vivo. Thus, we tested the effects of CRP administration on superoxide anion release and tissue factor activity and examined mechanistic pathways using a rat sterile air pouch model. Intraperitoneal administration of CRP (20 mg/kg body weight) compared to human serum albumin (HuSA) increased superoxide anion release and tissue factor activity from peritoneal macrophages in vivo (p < 0.01). This was confirmed using intrapouch administration of CRP (25 μg/mL) compared to HuSA. Pretreatment with reactive oxygen species (ROS) scavengers or protein kinase C (PKC) inhibitor significantly abrogated CRP-induced superoxide anion release and tissue factor activity. Pretreatment with extracellular signal-regulated kinase (ERK) and Jun N-terminal kinase (JNK) inhibitors, but not p38 mitogen-activated protein kinase (p38MAPK) significantly decreased CRP-induced superoxide anion release from macrophages in vivo. CRP-induced tissue factor activity in vivo was abrogated by pretreatment with inhibitors to p38MAPK, JNK and NFκb (nuclear factor-κb), but not ERK. Antibodies to Fc gamma receptors, CD32 and CD64 resulted in significant reduction in CRP-induced superoxide and tissue factor activity in vivo. Thus, CRP appears to induce oxidative stress in vivo by stimulating NADPH oxidase via PKC, ERK and JNK phosphorylation, and induces tissue factor PCA in vivo via upregulation of PKC, p38MAPK, JNK, ROS and NFκb. CRP-induced ROS appears to precede tissue factor release. These effects are abrogated by blocking Fc gamma receptors, CD32 and CD64. This in vivo demonstration provides further evidence for a role for CRP in atherothrombosis.

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Section: Discussionmentioning

confidence: 90%

C-reactive protein stimulates superoxide anion release and tissue factor activity in vivo

et al. 2009

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“…It has been suggested that a glucose-induced impairment of dimethylarginine dimethylaminohydrolase causes ADMA accumulation and may contribute to endothelial vasodilator dysfunction in diabetes mellitus [22]. C-reactive protein is a well-studied inflammatory marker in the setting of cardiovascular disease; and lastly, it has been suggested that increased CRP has also been associated with endothelial dysfunction and the progression of atherosclerosis [23]. In our study, plasma baseline CRP concentrations were increased at the prediabetic state, glucose loading caused an elevation in plasma CRP concentrations, and plasma CRP levels were found to be correlated with plasma ADMA levels at the prediabetic state.…”

Section: Discussionmentioning

confidence: 99%

The relationship between plasma asymmetrical dimethyl-l-arginine and inflammation and adhesion molecule levels in subjects with normal, impaired, and diabetic glucose tolerance

2008

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“…One theory is that renal dysfunction is related to inflammation through the reduction in the nitric oxide synthase activity [26]. Nitric oxide synthase is linked to inflammation through its role in the formation of peroxynitrate, an important mediator of the immune response.…”

Section: Discussionmentioning

confidence: 99%

The relation of C - reactive protein to chronic kidney disease in African Americans: the Jackson Heart Study

et al. 2010

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BackgroundAfrican Americans have an increased incidence and worse prognosis with chronic kidney disease (CKD - estimated glomerular filtration rate [eGFR] <60 ml/min/1.73 m2) than their counterparts of European-descent. Inflammation has been related to renal disease in non-Hispanic whites, but there are limited data on the role of inflammation in renal dysfunction in African Americans in the community.MethodsWe examined the cross-sectional relation of log transformed C-reactive protein (CRP) to renal function (eGFR by Modification of Diet and Renal Disease equation) in African American participants of the community-based Jackson Heart Study's first examination (2000 to 2004). We conducted multivariable linear regression relating CRP to eGFR adjusting for age, sex, body mass index, systolic and diastolic blood pressure, diabetes, total/HDL cholesterol, triglycerides, smoking, antihypertensive therapy, lipid lowering therapy, hormone replacement therapy, and prevalent cardiovascular disease events. In a secondary analysis we assessed the association of CRP with albuminuria (defined as albumin-to-creatinine ratio > 30 mg/g).ResultsParticipants (n = 4320, 63.2% women) had a mean age ± SD of 54.0 ± 12.8 years. The prevalence of CKD was 5.2% (n = 228 cases). In multivariable regression, CRP concentrations were higher in those with CKD compared to those without CKD (mean CRP 3.2 ± 1.1 mg/L vs. 2.4 ± 1.0 mg/L, respectively p < 0.0001). CRP was significantly associated with albuminuria in sex and age adjusted model however not in the multivariable adjusted model (p > 0.05).ConclusionCRP was associated with CKD however not albuminuria in multivariable-adjusted analyses. The study of inflammation in the progression of renal disease in African Americans merits further investigation.

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Nitric oxide and superoxide in rat mesangial cells: modulation by C-reactive protein

Cited by 11 publications

References 44 publications

C-reactive protein stimulates superoxide anion release and tissue factor activity in vivo

C-reactive protein stimulates superoxide anion release and tissue factor activity in vivo

The relationship between plasma asymmetrical dimethyl-l-arginine and inflammation and adhesion molecule levels in subjects with normal, impaired, and diabetic glucose tolerance

The relation of C - reactive protein to chronic kidney disease in African Americans: the Jackson Heart Study

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