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Effects of exercise training and antioxidant supplementation on endothelial cell gene expression

ABSTRACT: The molecular mechanisms of exercise-induced cardiovascular protection are poorly understood. There is growing evidence that reactive oxygen species (ROS) are necessary for some of these adaptations and antioxidants may be used to investigate this effect. This study aimed to determine the effects of exercise and/or antioxidant supplementation on myocardial and vascular endothelium gene expression. Male Wistar rats were divided into four groups: i) endurance exercise (90min of treadmill running 4d/week, 14 weeks); ii) antioxidant-treated; iii) antioxidant and endurance exercise and iv) control. The supplemented animals received Vitamin E (1000 IU/kg diet) and alpha-lipoic acid (1.6 g/kg diet) mixed with rat chow. cDNA microarray analysis was performed using purified endothelial RNA from myocardial and coronary artery endothelial cells and showed that the expression levels of 35, 40 and 40 genes were altered for groups i, ii, and iii respectively compared to control. Differentially expressed genes were analysed using the KEGG pathway database, hierarchical cluster and DAVID analysis. These analyses revealed that a gene involved in cardiovascular disease progression, Ras homolog gene family member A (RhoA) was down-regulated by exercise, upregulated by antioxidant supplementation and the combination of exercise and antioxidant blunted both effects. These findings were confirmed by real-time PCR. In summary, exercise and antioxidant supplementation affect endothelial cell gene expression and ROS appear necessary for some of these adaptations.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE14044 | GEO | 2009/12/18

SECONDARY ACCESSION(S): PRJNA112403

REPOSITORIES: GEO

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Project description:The molecular mechanisms of exercise-induced cardiovascular protection are poorly understood. There is growing evidence that reactive oxygen species (ROS) are necessary for some of these adaptations and antioxidants may be used to investigate this effect. This study aimed to determine the effects of exercise and/or antioxidant supplementation on myocardial and vascular endothelium gene expression. Male Wistar rats were divided into four groups: i) endurance exercise (90min of treadmill running 4d/week, 14 weeks); ii) antioxidant-treated; iii) antioxidant and endurance exercise and iv) control. The supplemented animals received Vitamin E (1000 IU/kg diet) and ï¡-lipoic acid (1.6 g/kg diet) mixed with rat chow. cDNA microarray analysis was performed using purified endothelial RNA from myocardial and coronary artery endothelial cells and showed that the expression levels of 35, 40 and 40 genes were altered for groups i, ii, and iii respectively compared to control. Differentially expressed genes were analysed using the KEGG pathway database, hierarchical cluster and DAVID analysis. These analyses revealed that a gene involved in cardiovascular disease progression, Ras homolog gene family member A (RhoA) was down-regulated by exercise, upregulated by antioxidant supplementation and the combination of exercise and antioxidant blunted both effects. These findings were confirmed by real-time PCR. In summary, exercise and antioxidant supplementation affect endothelial cell gene expression and ROS appear necessary for some of these adaptations. 48 Male Wistar rats were divided into four groups: i) endurance exercise (90min of treadmill running 4d/week, 14 weeks); ii) antioxidant-treated; iii) antioxidant and endurance exercise and iv) control. The supplemented animals received Vitamin E (1000 IU/kg diet) and ï¡-lipoic acid (1.6 g/kg diet) mixed with rat chow. cDNA microarray analysis was performed using purified endothelial RNA from myocardial and coronary artery endothelial cells. Based on the limited material available, it was necessary to combine the RNA into three pools per treatment group for CAEC (approx 400 ng of total RNA), and four pools for LVEC (approx 1 Î¼g of total RNA) with an additional reference pool from each control group.

Project description:Exercise is a fundamental component of human health that is associated with greater life expectancy and reduced risk of chronic diseases. While the beneficial effects of endurance exercise on human health are well established, the molecular mechanisms responsible for these observations remain unclear. Endurance exercise reduces the accumulation of mitochondrial DNA (mtDNA) mutations, alleviates multisystem pathology, and increases the lifespan of the mtDNA mutator mouse model of aging, in which the proof-reading capacity of mitochondrial polymerase gamma (POLG1) is deficient. Clearly, exercise recruited a POLG1-independent mtDNA repair pathway to induce these adaptations, a novel finding as POLG1 is canonically considered to be the sole mtDNA repair enzyme. Here we investigate the identity of this pathway, and show that endurance exercise prevents mitochondrial oxidative damage, attenuates telomere erosion, and mitigates cellular senescence and apoptosis in mtDNA mutator mice. Unexpectedly, we observe translocation of tumour suppressor protein p53 to mitochondria in response to endurance exercise that facilitates mtDNA mutation repair. Indeed, endurance exercise failed to prevent mtDNA mutations, induce mitochondrial biogenesis, preserve mitochondrial morphology, reverse sarcopenia, and mitigate premature mortality in mtDNA mutator mice with muscle-specific deletion of p53. Our data establish an exciting new role for p53 in exercise-mediated maintenance of the mtDNA genome, and presents mitochondrially-targeted p53 as a novel therapeutic modality for aging-associated diseases of mitochondrial etiology. Microarray analysis of gene expression from skeletal muscle (quadriceps femoris) from Mus musculus. N=23 samples per treatment were analysed for whole transcriptiome gene expression profile using NimbleGen Arrays. The treatment groups included wild-type C57Bl/6J mice as the control group, then two treatment groups which both contained homozygous knock-in mtDNA mutator mice (PolG; PolgAD257A/D257A). Once group of these heterozygous knock out mice received regular endurance exercise sessions while the other group remained sedentraty for 6 months. The control group specimens were wild-type litter mates to the transgenic knockout mice.

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Effects of exercise training and antioxidant supplementation on endothelial cell gene expression

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