scholarly journals Advanced Oxidation Protein Products Induce Inflammatory Response in Fibroblast-Like Synoviocytes through NADPH Oxidase -Dependent Activation of NF-κB

2013 ◽  
Vol 32 (4) ◽  
pp. 972-985 ◽  
Author(s):  
Shuai Zheng ◽  
Zhao-Ming Zhong ◽  
Shuai Qin ◽  
Guo-Xian Chen ◽  
Qian Wu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Nadph Oxidase ◽  
Advanced Oxidation ◽  
Advanced Oxidation Protein Products ◽  
Fibroblast Like Synoviocytes

Advanced oxidation protein products and inflammatory markers in liver cirrhosis: a comparison between alcohol-related and HCV-related cirrhosis.

2011 ◽  
Vol 58 (1) ◽  
Author(s):  
Jolanta Zuwała-Jagiełło ◽  
Monika Pazgan-Simon ◽  
Krzysztof Simon ◽  
Maria Warwas
Keyword(s):  
Oxidative Stress ◽  
Liver Cirrhosis ◽  
Inflammatory Response ◽  
Chronic Inflammation ◽  
Inflammatory Markers ◽  
Antioxidant Defense ◽  
Early Stage ◽  
Plasma Concentrations ◽  
Advanced Oxidation ◽  
Advanced Oxidation Protein Products

Advanced oxidation protein products (AOPPs) are protein markers of oxidative stress with pro-inflammatory properties that accumulated in liver cirrhosis. In the present study, we investigated the association between chronic inflammatory response triggered by AOPPs and the severity of liver disease as assessed by the Child-Pugh score. Plasma concentrations of AOPPs and inflammatory markers such as C-reactive protein, tumor necrosis factor-α, and interleukin-6 were measured in 41 patients with HCV-related cirrhosis, 43 patients with alcohol-related liver cirrhosis (ALC), and in 30 age and sex matched controls. In comparison with controls, AOPPs were increased in HCV-related compensated (Child-Pugh A) and decompensated (Child-Pugh B-C) cirrhosis and in alcohol-related compensated cirrhosis. AOPPs level positively correlated with Child-Pugh score in alcohol-related cirrhosis but not in HCV-related cirrhosis and the correlation with the indices of chronic inflammation was stronger in ALC. In turn, AOPPs in HCV-related cirrhosis was related to inflammation to a lesser extent, but a significant correlation with antioxidant defense could be noted. In summary, liver cirrhosis was associated with increased formation of AOPPs, which differed between alcohol-related and HCV-related cirrhosis with respect to the relationship between AOPPs and antioxidant defense, stage of liver cirrhosis, and inflammatory response. The significant correlation between AOPPs accumulation and indices of chronic inflammation, more specifically TNF-α, suggests that oxidative stress may be a mediator of chronic inflammatory state in the early stage of alcohol-related cirrhosis.

Advanced oxidation protein products induce mesangial cell perturbation through PKC-dependent activation of NADPH oxidase

2009 ◽  
Vol 296 (2) ◽  
pp. F427-F437 ◽  
Author(s):  
Xiao Fan Wei ◽  
Qiu Gen Zhou ◽  
Fan Fan Hou ◽  
Bei Yi Liu ◽  
Min Liang
Keyword(s):  
Nadph Oxidase ◽  
Mesangial Cells ◽  
Advanced Oxidation ◽  
Advanced Oxidation Protein Products ◽  
Glomerular Diseases ◽  
Regulatory Subunits ◽  
New Information ◽  
Pathogenic Factors ◽  
Underlying Mechanisms ◽  
Membrane Components

Mesangial deposition of extracellular matrix (ECM) is a hallmark of several glomerular diseases including diabetic nephropathy. Accumulation of advanced oxidation protein products (AOPPs) has been found in diabetes and chronic kidney disease and linked to mesangial ECM deposition and progressive glomerulosclerosis in these disorders. Although emerging evidence implicates AOPPs as the renal pathogenic factors, the underlying mechanisms have not been investigated. Here, using cultured rat mesangial cells (MCs) as a model, we identify AOPPs as the important mediators for activation of MC NADPH oxidase. Exposure of MCs to AOPPs, through membrane-associated phosphorylation of PKCα, induced rapid phosphorylation of cytosolic p47phox and its membrane translocation, enhanced interaction of p47phox with the membrane components p22phox and Nox4, and increased expression of these key regulatory subunits of NADPH oxidase. Challenge with AOPPs triggered cytosolic superoxide generation, resulting in upregulation of fibronectin and collagen IV genes and proteins and overexpression of TGF-β1 via a PKC-NADPH oxidase-dependent pathway, as these downstream events were blocked by the inhibitors of PKC, inhibitors of NADPH oxidase, or the cytosolic superoxide scavenger. These data provide new information for understanding the molecular basis underlying AOPP-induced MC perturbation and might be a central step toward development of new interventions.

scholarly journals Age-related accumulation of advanced oxidation protein products promotes osteoclastogenesis through disruption of redox homeostasis

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Jingshen Zhuang ◽  
Xuebing Chen ◽  
Guixing Cai ◽  
Dizheng Wu ◽  
Chen Tu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Loss ◽  
Nadph Oxidase ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Advanced Oxidation ◽  
Oxidase Inhibitor ◽  
Nuclear Factor ◽  
Advanced Oxidation Protein Products ◽  
Age Related

AbstractEnhanced osteoclastogenesis is one of the major causes of age-related bone loss. Aging is accompanied by accumulation of advanced oxidation protein products (AOPPs). However, whether AOPPs accumulation contributing to the osteoclastogenesis with aging remains unclear. Here, we showed that AOPPs accumulation was associated with the enhanced osteoclastogenesis and deterioration of bone microstructure in aged mice. In vitro, AOPPs directly induced osteoclastogenesis by interaction with receptor activator of nuclear factor κ B (RANK) and the receptor for advanced glycation end products (RAGE) in the primary bone marrow monocytes. Bindings of AOPPs to RANK and RAGE were able to activate nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, trigger generation of reactive oxygen species, then induce phosphorylation of mitogen-activated protein kinases and c-fos, upregulation of the nuclear factor of activated T cell c1, eventually induce bone marrow monocytes to differentiate into mature osteoclasts. Chronic exposure to AOPPs enhanced osteoclastogenesis and bone loss in mice, which could be alleviated by NADPH oxidase inhibitor apocynin. Local injection of AOPPs into subperiosteal area induced bone resorption at the site of administration, which was similar to the effect of RANK ligand. Together, these results suggested that AOPPs could serve as a novel regulator of osteoclastogenesis and AOPPs accumulation might play an important role in the development of age-related bone loss.

scholarly journals Advanced Oxidation Protein Products Promote Inflammation in Diabetic Kidney through Activation of Renal Nicotinamide Adenine Dinucleotide Phosphate Oxidase

Endocrinology ◽  
2008 ◽  
Vol 149 (4) ◽  
pp. 1829-1839 ◽  
Author(s):  
Xiao Yun Shi ◽  
Fan Fan Hou ◽  
Hong Xin Niu ◽  
Guo Bao Wang ◽  
Di Xie ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Advanced Oxidation ◽  
Diabetic Rats ◽  
Nicotinamide Adenine ◽  
Control Group ◽  
Advanced Oxidation Protein Products ◽  
Renal Inflammation ◽  
Diabetic Kidney

The involvement of inflammatory processes has been recognized in development and/or progression of diabetic nephropathy. However, the mechanisms involved in the pathogenesis of renal inflammation have not been completely understood. In this study, we tested the hypothesis that accumulation of advanced oxidation protein products (AOPPs), which occurs in diabetes, may promote inflammatory responses in diabetic kidney. Streptozotocin-induced diabetic rats were randomized to iv injection of vehicle, native rat serum albumin (RSA), and AOPPs-modified RSA (AOPPs-RSA) in the presence or absence of oral administration of apocynin. A control group was followed concurrently. Compared with RSA- or vehicle-treated diabetic rats, AOPPs-RSA-treated animals displayed significant increase in renal macrophage infiltration and overexpression of monocyte chemoattractant protein-1 and TGF-β1. This was associated with deteriorated structural and functional abnormalities of diabetic kidney, such as glomerular hypertrophy, fibronectin accumulation, and albuminuria. AOPP challenge significantly increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent superoxide generation in renal homogenates and up-regulated membrane expression of renal NADPH oxidase subunits p47phox and gp91phox. All these AOPPs-induced perturbations in diabetic kidney could be prevented by the NADPH oxidase inhibitor apocynin. These data suggest that chronic accumulation of AOPPs may promote renal inflammation in diabetes probably through activation of renal NADPH oxidase.

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