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Khaper, Neelam; Kaur, Kuljeet; Li, T.; Farahmand, Firoozeh; Singal, Pawan K.

doi:10.1023/a:1025448908694

Cited by 62 publications

(18 citation statements)

References 39 publications

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“…The mechanisms for the changes in SOD levels in the repairing kidney remain to be elucidated. Studies have shown that SOD is decreased in the repairing heart and kidney [23, 24]. Thus, renal oxidative stress in this model of hypertension is induced by both upregulated ROS production and reduced antioxidant enzyme in the kidney.…”

Section: Discussionmentioning

confidence: 93%

Kidney Fibrosis in Hypertensive Rats: Role of Oxidative Stress

Zhao¹,

Chen

et al. 2008

Am J Nephrol

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Fibrosis of the glomerulus and the tubulointerstitium occurs in patients with hypertension. Studies have shown that renal oxidative stress appears in hypertensive kidney disease. The potential role of oxidative stress in renal fibrogenesis remains to be elucidated. Herein, we tested the hypothesis that oxidative stress contributes to the development of renal fibrosis during hypertension.Sprague-Dawley rats received angiotensin II (AngII; 9 µg/h s.c.) for 4 weeks with/without co-treatment of antioxidants, apocynin and tempol (120 mg/kg/day each, p.o.). Untreated rats served as controls. Appearance of renal oxidative stress and its effect on the expression of transforming growth factor (TGF)-β₁, population of myofibroblasts, collagen synthesis/degradation and fibrosis in kidneys were examined. Chronic AngII infusion elevated systemic blood pressure (228 ± 6 mm Hg), which was accompanied with extensive renal fibrosis and oxidative stress represented as upregulated NADPH oxidase and suppressed superoxide dismutase (SOD). Co-treatment with antioxidants led to: (1) markedly decreased renal NADPH oxidase; (2) significantly attenuated gene expression of TGF-β₁, type I collagen, and tissue inhibitors of matrix metalloproteinase (TIMP)-I/-II in the kidney; (3) largely reduced population of myofibroblasts in both the cortex and medulla; (4) significantly reduced renal collagen volume, and (5) partially suppressed blood pressure (190 ± 8 mm Hg). Thus, prolonged AngII administration promotes renal oxidative stress, which is associated with hypertensive renal disease. AngII induces renal oxidative stress by increasing NADPH oxidase and reducing SOD in the kidney, which, in turn, upregulates collagen synthesis, while suppressing collagen degradation, thereby promoting the development of fibrosis in kidneys of hypertensive rats.

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Section: Discussionmentioning

confidence: 93%

Kidney Fibrosis in Hypertensive Rats: Role of Oxidative Stress

Zhao¹,

Chen

et al. 2008

Am J Nephrol

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“…Interestingly, we found to be a downregulation of SOD1 mRNA after MI procedures compared to control. SOD1 gene overexpression also elevated levels of myocyte catalase and mitochondrial GSH, which might also act together with SOD1 against oxidative stress (Khaper et al, 2003). Catalase gene was differently expressed in each procedure compared to control.…”

Section: Discussionmentioning

confidence: 99%

Comparative mRNA and MicroRNA Profiling during Acute Myocardial Infarction Induced by Coronary Occlusion and Ablation Radio-Frequency Currents

et al. 2016

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The ligation of the left anterior descending coronary artery is the most commonly used experimental model to induce myocardial infarction (MI) in rodents. A high mortality in the acute phase and the heterogeneity of the size of the MI obtained are drawbacks recognized in this model. In an attempt to solve the problem, our group recently developed a new MI experimental model which is based on application of myocardial ablation radio-frequency currents (AB-RF) that yielded MI with homogeneous sizes and significantly reduce acute mortality. In addition, cardiac structural, and functional changes aroused by AB-RF were similar to those seen in animals with MI induced by coronary artery ligation. Herein, we compared mRNA expression of genes that govern post-MI milieu in occlusion and ablation models. We analyzed 48 mRNAs expressions of nine different signal transduction pathways (cell survival and metabolism signs, matrix extracellular, cell cycle, oxidative stress, apoptosis, calcium signaling, hypertrophy markers, angiogenesis, and inflammation) in rat left ventricle 1 week after MI generated by both coronary occlusion and AB-RF. Furthermore, high-throughput miRNA analysis was also assessed in both MI procedures. Interestingly, mRNA expression levels and miRNA expressions showed strong similarities between both models after MI, with few specificities in each model, activating similar signal transduction pathways. To our knowledge, this is the first comparison of genomic alterations of mRNA and miRNA contents after two different MI procedures and identifies key signaling regulators modulating the pathophysiology of these two models that might culminate in heart failure. Furthermore, these analyses may contribute with the current knowledge concerning transcriptional and post-transcriptional changes of AB-RF protocol, arising as an alternative and effective MI method that reproduces most changes seem in coronary occlusion.

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“…Khaper et al . followed the expression of various antioxidant enzymes, including MnSOD, at different times following myocardial infarction in rats, and found that MnSOD mRNA levels were reduced early (1 week) and long after (16 weeks) infarction, but MnSOD mRNA was near control levels at 4 weeks post-infarction [356]. …”

Section: Implications For Diseasementioning

confidence: 99%

Manganese Superoxide Dismutase: Guardian of the Powerhouse

Holley

Bakthavatchalu

Velez-Roman

et al. 2011

IJMS

257

180

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The mitochondrion is vital for many metabolic pathways in the cell, contributing all or important constituent enzymes for diverse functions such as β-oxidation of fatty acids, the urea cycle, the citric acid cycle, and ATP synthesis. The mitochondrion is also a major site of reactive oxygen species (ROS) production in the cell. Aberrant production of mitochondrial ROS can have dramatic effects on cellular function, in part, due to oxidative modification of key metabolic proteins localized in the mitochondrion. The cell is equipped with myriad antioxidant enzyme systems to combat deleterious ROS production in mitochondria, with the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) acting as the chief ROS scavenging enzyme in the cell. Factors that affect the expression and/or the activity of MnSOD, resulting in diminished antioxidant capacity of the cell, can have extraordinary consequences on the overall health of the cell by altering mitochondrial metabolic function, leading to the development and progression of numerous diseases. A better understanding of the mechanisms by which MnSOD protects cells from the harmful effects of overproduction of ROS, in particular, the effects of ROS on mitochondrial metabolic enzymes, may contribute to the development of novel treatments for various diseases in which ROS are an important component.

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Untitled

Cited by 62 publications

References 39 publications

Kidney Fibrosis in Hypertensive Rats: Role of Oxidative Stress

Kidney Fibrosis in Hypertensive Rats: Role of Oxidative Stress

Comparative mRNA and MicroRNA Profiling during Acute Myocardial Infarction Induced by Coronary Occlusion and Ablation Radio-Frequency Currents

Manganese Superoxide Dismutase: Guardian of the Powerhouse

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