The molecular sources of reactive oxygen species in hypertension

Puddu, Paolo; Puddu, Giovanni M.; Cravero, Eleonora; Rosati, M.; Muscari, Antonio

doi:10.1080/08037050802029954

Cited by 65 publications

(35 citation statements)

References 98 publications

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“…The AGEs-RAGE axis may induce intracellular ROS formation, stimulating NADPH oxidase (Wautier et al 2001). In addition, other sources of ROS have been reported, including nitric oxide synthase, cytochrome P450 oxidase and several other enzymes, which may contribute to the generation of intracellular O 2 _ and H 2 O 2 in monocytes, ECs, and VSMCs (Puddu et al 2008). Our data showed that the glycol-AGEs-induced ROS generation was mainly derived from both the mitochondrial respiratory chain and NADPH oxidase in ECs (Figure 1(D)).…”

Section: Discussionmentioning

confidence: 99%

Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium

Nam

Son

Lee

et al. 2015

Cell Communication & Adhesion

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Advanced glycation end-products (AGEs) are involved in the development of vascular smooth muscle cell (VSMC) dysfunction and the progression of atherosclerosis. However, AGEs may indirectly affect VSMCs via AGEs-induced signal transduction between monocytes and human umbilical endothelial cells (HUVECs), rather than having a direct influence. This study was designed to elucidate the signaling pathway underlying AGEs-RAGE axis influence on VSMC dysfunction using a co-culture system with monocytes, HUVECs and VSMCs. AGEs stimulated production of reactive oxygen species and pro-inflammatory mediators such as tumor necrosis factor-a and interleukin1b via extracellular-signal-regulated kinases phosphorylation and nuclear factor-jB activation in HUVECs. It was observed that AGEs-induced pro-inflammatory cytokines increase VSMC proliferation, inflammation and vascular remodeling in the co-culture system. This result implies that RAGE plays a role in AGEs-induced VSMC dysfunction. We suggest that the regulation of signal transduction via the AGEs-RAGE axis in the endothelium can be a therapeutic target for preventing atherosclerosis.ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium

Nam

Son

Lee

et al. 2015

Cell Communication & Adhesion

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“…2D) in this study. The development of hypertension induces an increase in reactive oxygen species (ROS) levels, suggesting that excessive endothelial ROS production is a causal factor of hypertension, which induces damage to the vasculature 25) . Therefore, hypertension in SHR and CP groups may be associated with increased oxidative stress and decreased nitric oxide.…”

Section: Discussionmentioning

confidence: 99%

Skeletal Muscle Characteristics of Rats with Obesity, Diabetes, Hypertension, and Hyperlipidemia

Nagatomo

Fujino

et al. 2009

JAT

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Aim: Data on the skeletal muscle characteristics of patients and animals with lifestyle-related diseases are limited. We investigated mRNA expression levels and fiber profiles in the skeletal muscles of rats with obesity, diabetes, hypertension, and/or hyperlipidemia. Methods: The mRNA expression levels of peroxisome proliferator-activated receptors (PPAR and PPAR / ), PPAR coactivator-1 (PGC-1 ), stearoyl-CoA desaturase-1 (SCD-1), carnitine palmitoyl-transferase (CPT ), medium-chain acyl-CoA dehydrogenase (MCAD), and mitochondrial transcriptional factor A (TFAM) in the soleus muscles were compared among 15-week-old control (WR), type 2 diabetic (GK), hypertensive (SHR), and hyperlipidemic (CP) rats. The fiber profiles in the soleus muscles of these rats were also determined. Results: GK rats showed lower PPAR / , PGC-1 , and MCAD expression levels than WR rats. SHR rats showed higher PPAR and MCAD and lower PPAR / expression levels than WR rats. CP rats showed lower PPAR / and higher SCD-1 expression levels than WR rats. The muscles of WR, SHR, and CP rats had low-oxidative type and high-oxidative type A and type C fibers, whereas the muscle of GK rats had only low-oxidative type fibers. Conclusions:The skeletal muscles of rats with lifestyle-related diseases have unique mRNA expression patterns and fiber profiles depending on the type of disease. For example, the lower PGC-1 and MCAD mRNA expression levels in the soleus muscles of type 2 diabetic rats are associated with the presence of only low-oxidative type fibers in the muscle. J Atheroscler Thromb, 2009; 16:576-585.Key words; Lifestyle-related disease, mRNA expression level, Muscle fiber type bility of ATPase at acidic pH. Type A fibers become ATPase negative at a faster rate than type B fibers when the acidity of the preincubation medium increases. Type C fibers have been identified in skeletal muscles, particularly in the soleus muscle of rats; these fibers are ATPase positive, irrespective of the pH of the preincubation medium. Glycolytic enzyme activity is higher in type A, type B, and type C fibers than in type fibers, whereas oxidative enzyme activity is higher in type , type A, and type C fibers than in type B fibers; therefore, the presence of different types of fibers correlates with the metabolic properties of individual skeletal muscles. Skeletal muscles exhibit plasticity and undergo fiber type transitions under various conditions, such as growth, aging,

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“…It has been reported that reactive oxygen species (ROS) and advanced glycation end products (AGEs) might be involved in the regulation of ABC transporters through LXR-independent mechanisms. 19,20 In both animal models and in humans, increased blood pressure has been associated with oxidative stress and the generation of ROS; 21 ROS is involved in the downregulation of ABCA1 expression in macrophages, 19 which might be a potential underlying mechanism, whereby the expression of ABCA1 decreased in hypertensive conditions. AGEs are also associated with hypertension, 22 and may reduce the expression of ABCG1 in vitro, 20 as well as in type II diabetic patients.…”

Section: Discussionmentioning

confidence: 99%

The expression of ATP-binding cassette transporters in hypertensive patients

Zhou

et al. 2009

Hypertens Res

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Cholesterol efflux is regulated by cholesterol transporters, including adenosine triphosphate-binding cassette transporters, A1, G1 (ABCA1, ABCG1), and scavenger receptor class B type I (SR-BI). We have investigated whether the expression of these transporters/receptor is altered in patients with hypertension and also studied their functional effects in cholesterol efflux. The newly diagnosed hypertensive patients, as well as age-and gender-matched healthy controls were recruited. mRNA of ABCA1, ABCG1 and SR-BI in monocytes was measured. The functional effects of the three transporters/receptor and cholesterol efflux from monocyte-derived macrophages ex vivo were also determined. The expression of ABCA1 and ABCG1 was significantly decreased in the newly diagnosed untreated hypertensive patients compared with that in healthy controls. The levels of ABCA1 and ABCG1 were negatively associated with blood pressure, and the reduction of ABCA1 and ABCG1 could be reversed by antihypertensive therapy. No significant associations between plasma lipids, oxidized low-density lipoprotein (LDL) and the expression of ABCA1 or ABCG1 were found. Cholesterol efflux from monocyte-derived macrophages to autologous serum, apolipoprotein AI (apoAI) or high-density lipoprotein (HDL) was impaired in hypertensive patients. Cholesterol efflux to autologous serum or apoAI was associated with the expression of ABCA1, whereas cholesterol efflux to autologous serum or HDL was associated with the expression of ABCG1. The expression of ABCA1 and ABCG1 in monocytes is reduced in hypertensive patients, which could be reversed by anti-hypertensive therapy. The reduction in ABCA1/ABCG1 is associated with the impairment of cholesterol efflux from monocyte-derived macrophages.

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The molecular sources of reactive oxygen species in hypertension

Cited by 65 publications

References 98 publications

Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium

Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium

Skeletal Muscle Characteristics of Rats with Obesity, Diabetes, Hypertension, and Hyperlipidemia

The expression of ATP-binding cassette transporters in hypertensive patients

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