MyomiRs in cultured muscle cells from patients with idiopathic inflammatory myopathy are modulated by disease but not by 6-month exercise training.

Objectives: Idiopathic inflammatory myopathies/IIM are associated with changes in muscle-specific microRNA/miR. Exercise improves muscle function and metabolism in parallel with changes in miR expression. We investigated the effects of disease and exercise on miRs in differentiated muscle cells/myotubes from IIM patients and controls.

Clusterin is upregulated in serum and muscle tissue in idiopathic inflammatory myopathies and associates with clinical disease activity and cytokine profile.

Objectives: The aim of this cross-sectional study was to explore the circulating and skeletal muscle expression of clusterin (CLU) in inflammatory myopathies (IIM) and its potential implication in pathogenetic mechanisms of the disease.

Methods: A total of 85 IIM patients and 86 healthy controls (HC) were recruited. In addition, 20 IIM patients and 21 HC underwent a muscle biopsy.

Alterations in activin A-myostatin-follistatin system associate with disease activity in inflammatory myopathies.

Objectives: The aim of this study was to investigate the systemic and skeletal muscle levels of atrophy-associated myokines in patients with idiopathic inflammatory myopathies (IIM) and their association with clinical characteristics of myositis.

Methods: A total of 94 IIM patients and 162 healthy controls were recruited. Of those, 20 IIM patients and 28 healthy controls underwent a muscle biopsy.

Inhibition of mitochondrial glycerol-3-phosphate dehydrogenase by α-tocopheryl succinate.

α-Tocopheryl succinate (TOS), a redox-silent analogue of vitamin E, suppresses cell growth in a number of clinical and experimental cancers, inhibits mitochondrial succinate dehydrogenase (SDH) and activates reactive oxygen species (ROS) generation. The aim of this study was to test whether TOS also inhibits glycerol-3-phosphate dehydrogenase (mGPDH), another flavoprotein-dependent enzyme of the mitochondrial respiratory chain because there are differences between electron transfer pathway from SDH and mGPDH to coenzyme Q pool. For our experiments brown adipose tissue mitochondria with high expression of mGPDH were used.

Endothelial cells negatively modulate reactive oxygen species generation in vascular smooth muscle cells: role of thioredoxin.

In intact vessels, endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) act as an integrated system, possibly through reactive oxygen species (ROS). Using a coculture system we tested whether ECs modulate VSMC redox status by regulating activity of NAD(P)H oxidase and antioxidants. VSMC production of O(2)(*-), H(2)O(2), and NO was assessed using fluoroprobes and amplex-red.

Reactive oxygen species, cell growth, cell cycle progression and vascular remodeling in hypertension.

Reactive oxygen species (ROS) include superoxide, hygrogen peroxide and hydroxyl radical. Under physiological conditions, all vascular cell types produce ROS in a controlled and regulated fashion, mainly through nonphagocyte NADPH oxidase. An imbalance between pro-oxidants and antioxidants results in oxidative stress.

Activity of lactate dehydrogenase in serum and cerebral cortex of immature and mature rats after hypobaric hypoxia.

In our previous studies we have found both an increase of lipid peroxidation damage (expressed as levels of thiobarbituric acid-reactive substances) in brain and plasma lactate concentration in 21-day-old rats after a 30-min exposure to hypobaric hypoxia. Pretreatment of rats with L-carnitine decreased both parameters. The aim of our present study was to determine if the L-carnitine-dependent decrease of plasma lactate could be due to a modification of lactate dehydrogenase (LDH) activity.

Chronic N-acetylcysteine administration prevents development of hypertension in N(omega)-nitro-L-arginine methyl ester-treated rats: the role of reactive oxygen species.

The aim of this study was to evaluate the production of superoxide anions as well as their role in the induction and/or maintenance of high blood pressure in rats with N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. In the preventive study, we compared adult Wistar rats treated with L-NAME for 4 weeks with L-NAME-treated rats that were simultaneously given N-acetylcysteine (NAC) in their drinking water. Basal blood pressure, superoxide production, conjugated dienes concentration and NO synthase (NOS) activity were measured at the end of the experiment.

Relationships between membrane lipids and ion transport in red blood cells of Dahl rats.

Distinct changes of membrane lipid content could contribute to the abnormalities of ion transport that take part in the development of salt hypertension in Dahl rats. The relationships between lipid content and particular ion transport systems were studied in red blood cells (RBC) of Dahl rats kept on low- and high-salt diets for 5 weeks since weaning. Dahl salt-sensitive (SS/Jr) rats on high-salt diet had increased blood pressure, levels of plasma triacylglycerols and total plasma cholesterol compared to salt-resistant (SR/Jr) rats.

Membrane ion transport in erythrocytes of salt hypertensive Dahl rats and their F2 hybrids: the importance of cholesterol.

The possible association of salt hypertension and altered lipid metabolism with abnormalities of particular systems transporting sodium and potassium has been studied in erythrocytes of Dahl rats and their F2 hybrids fed a high-salt diet since weaning. Our attention was paid to the Na(+)-K+ pump, Na(+)-K+ cotransport and especially to passive membrane permeability for Na+ and Rb+ (Na+ and Rb+ leak), because the Na+ leak was found to be dependent on the genotype, age and salt intake of Dahl rats, whereas the Rb+ leak was suggested to be a potential marker of salt sensitivity in Dahl and Sabra rats. Young male Dahl salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) rats kept on a low-salt (0.

Erythrocyte ion transport and membrane lipid composition in young and adult rats with NO-deficient hypertension.

The aim of our study was to search for abnormalities of sodium and potassium transport in erythrocytes of male Wistar rats subjected to chronic L-NAME treatment (40 mg/kg/day) for 4 weeks either from weaning (4-week-old) or in adulthood (12-week-old). Sodium content, Na(+),K(+)-pump and Na(+),K(+)-cotransport activity, cation leaks as well as membrane cholesterol and phospholipid contents were determined in fresh erythrocytes. Chronic inhibition of NO synthase elicited similar blood pressure rise in both age groups which did not differ in the degree of NO synthase inhibition.

Effect of acute hyperglycemia on erythrocyte membrane ion transport in offspring of hypertensive parents.

Objective: Patients with essential hypertension exhibit several red blood cell (RBC) ion transport abnormalities, insulin resistance (IR) and increased risk of developing type 2 diabetes. The aims of this study were to assess RBC ion transport activities under basal conditions and to test the in vivo effect of acute hyperglycemia on RBC ion transport in the offspring of hypertensive parents (OHP) and healthy controls (C).

Design And Methods: Activities of Na+-K+ pump, Na+-K+ cotransport, Na+-Li+ countertransport (SLC) and Na+, Rb+ and Li+ leaks were measured before and after a 5-h hyperglycemic (12 mmol/l) clamp (HGC) and compared to values found under euglycemic isovolumic conditions in OHP (n = 12) and C (n = 14).

Erythrocyte membrane ion transport in offspring of hypertensive parents: effect of acute hyperinsulinemia and relation to insulin action.

Some patients with essential hypertension exhibit insulin resistance (IR) and several red blood cell (RBC) ion transport abnormalities. The aims of the study were to assess RBC ion transport acitivities under basal conditions, to test in vivo the effect of acute hyperinsulinemia, and to evaluate the relationship to IR in the offspring of hypertensive parents (n = 12; OHP) and healthy controls (n = 14; C). Activities of the Na+-K+ pump, Na+-K+ cotransport, Na+-Li+ countertransport (SLC), and Na+, Rb+, and Li+ leaks (passive membrane permeability) were measured before and after a hyperinsulinemic (75 microU/mL) euglycemic clamp (HIC) and compared to those found under isoinsulinemic isovolumic conditions in OHP and C.