Role of NAD(P)H oxidase in transforming growth factor‐β1‐induced monocyte chemoattractant protein‐1 and interleukin‐6 expression in rat renal tubular epithelial cells

Zhang, Haiyan; Jiang, Zongpei; Chang, Jie; Li, Xiaoyan; Zhu, Hengmei; Lan, Hui‐Yao; Zhou, Shu‐Feng; Yu, Xueqing

doi:10.1111/j.1440-1797.2008.01072.x

Cited by 19 publications

(13 citation statements)

References 31 publications

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“…There is accumulating evidence that aging is associated with a pro-inflammatory shift in vascular phenotype (Csizar et al, 2007), kidney (Rodwell et al, 2004), liver (Coban et al, 2008) and heart (Brinkley et al, 2009). We must comment that the presence of IL-6 in epithelial cells could be odd, but this result is in agreement with other data suggesting its expression in progressive renal disease (Zhang et al, 2009) presented an increased expression of IL-6. Increased production of ROS, normally due to a decrease of antioxidant enzymes (i.e.…”

supporting

confidence: 92%

Apolipoprotein E and its role in aging and survival

Bonomini

Filippini

Hayek

et al. 2010

Experimental Gerontology

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The study of biological aging has seen spectacular progress in the last decade and markers are increasingly employed for understanding physiological processes that change with age. Recently, it has been demonstrated that apolipoprotein E (apoE) has a major impact on longevity, but its mechanisms are still not fully understood. ApoE-deficient (E o ) mice have proved to be a very popular model for studying spontaneous hypercholesterolemia and the subsequent development of atherosclerotic lesions, but only limited data are available with regard to aging and aging changes.We used this murine model to better characterize the involvement of apoE in aging and to evaluate its role in the maintenance of normal organ morphology. Our results show that E 0 mice at different ages (6, 12, 20 weeks old) developed age-dependent morphological and biochemical alterations, including fibrosis (newly formed collagen), pro-inflammatory cytokine (IL-6 and iNOS), lipofuscin accumulation, and decrease of antioxidant enzymes (superoxide dismutase and catalase) in several organs (kidney, liver and heart). It is significant that the observed degenerative findings in E 0 mice at different ages (6, 12, 20 weeks old) were not identified in control mice (C57BL), at 6, 12 and 20 weeks of age. Consequently, since these mice showed enzymatic and structural alterations, normally linked to the age, such as increase of lipofuscin, pro-inflammatory cytokines and decrease of antioxidant enzymes, we can conclude that apoE is a useful player in studies of longevity and age-related diseases, such as inflammatory status and atherosclerosis that are known risk factors for functional decline and early mortality. Moreover, it is possible that apoE may also play a role in other pathological conditions including, for example, cancer, rheumatoid arthritis and macular degeneration.

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supporting

confidence: 92%

Apolipoprotein E and its role in aging and survival

Bonomini

Filippini

Hayek

et al. 2010

Experimental Gerontology

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“…can activate not only inflammatory cascades but can also contribute to the development of oxidative stress. Pro-inflammatory mediators (such as interleukin-6) can activate oxidative stress mechanisms such as NADPH oxidases leading to generation of ROS (80). Excess ROS can lead to mitochondrial dysfunction further promoting oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide, oxidative stress and inflammation in pulmonary arterial hypertension

Crosswhite

Sun

2010

Journal of Hypertension

154

137

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Pulmonary arterial hypertension (PAH) is a chronic and progressive disease characterized by a persistent elevation of pulmonary artery pressure accompanied by right ventricular hypertrophy (RVH). The current treatment for pulmonary hypertension is limited and only provides symptomatic relief due to unknown etiology and pathogenesis of the disease. Both vasoconstriction and structural remodeling (enhanced proliferation of VSMC) of the pulmonary arteries contribute to the progressive course of PAH, irrespective of different underlying causes. The exact molecular mechanism of PAH, however, is not fully understood. The purpose of this review is to provide recent advances in the mechanistic investigation of PAH. Specifically, this review focuses on nitric oxide (NO), oxidative stress and inflammation and how these factors contribute to the development and progression of PAH. This review also discusses recent and potential therapeutic advancements for the treatment of PAH.

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“…Oxidative stress is implicated in TGF-b-mediated tubular cell injury, with TGF-b having been shown to promote the upregulation of NADPH oxidase subunits in rat renal tubular cells [57]. Furthermore, in response to TGF-b, Nox-4 is the predominant isoform implicated in kidney myofibroblast differentiation and expression of fibronectin [38,58].…”

Section: Key Pointsmentioning

confidence: 99%