Regular treadmill exercise inhibits mitochondrial accumulation of cholesterol and oxysterols during myocardial ischemia-reperfusion in wild-type and ob/ob mice

Musman, Julien; Pons, Sandrine; Barau, Caroline; Caccia, Claudio; Leoni, Valerio; Berdeaux, Alain; Ghaleh, Bijan; Morin, Didier

doi:10.1016/j.freeradbiomed.2016.10.496

Cited by 24 publications

(15 citation statements)

References 42 publications

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“…Mitochondrial biogenesis is promoted via the activation of JAK/STAT by leptin, via downstream proteins, such as proliferator-activated receptor γ a co-activator-1α and mitochondrial transcription factor A. Such activation has been indicated to be involved in neuronal cell protection via the enhancement of anti-oxidant enzyme activities (15,47). It has been demonstrated that leptin increases superoxide dismutase (SOD) levels, stabilizes the mitochondrial membrane and alleviates endoplasmic reticulum pressure (17); this in turn inhibits the production of free radicals and ischemic injury in mice by binding to OB-Rb in the cortex, hippocampus and striatum.…”

Section: Protective Mechanisms Of Leptin In the Brainmentioning

confidence: 99%

“…Leptin receptors in locations including the striatum have protective roles (12). Studies have demonstrated considerable reductions in excitatory amino acids (EAAs) (13,14), oxygen free radicals, inflammatory factors (15–17), mitochondrial damage and apoptosis in leptin-preconditioned groups compared with those in untreated groups (Fig. 2).…”

Section: Introductionmentioning

confidence: 99%

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Protective effects of leptin against cerebral ischemia/reperfusion injury (Review)

Zhang

Jin

et al. 2019

Exp Ther Med

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In recent years, the use of thrombolytic therapy for treating ischemia/reperfusion injury has resulted in damage to the self-regulatory mechanisms of the brain. This is due to the increased production of free radicals, excitatory amino acids and pro-inflammatory cytokines causing secondary damage to the brain. Simple thrombolytic therapy has not been the best approach for treating ischemia/reperfusion injury. Excessive perfusion leads to failure of the body's self-regulatory functions, which in turn increases the area of cerebral edema and aggravates cerebral ischemia. Previous studies have evaluated the satiety hormone leptin as a link between energy expenditure and obesity. Of note, leptin, which is involved in brain development, synaptic transmission and angiogenesis following ischemia/reperfusion injury, has been considered an important factor for treating ischemia/reperfusion injury. The present review outlines the discovery of leptin and discusses its association with cerebral ischemia/reperfusion.

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Section: Protective Mechanisms Of Leptin In the Brainmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protective effects of leptin against cerebral ischemia/reperfusion injury (Review)

Zhang

Jin

et al. 2019

Exp Ther Med

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“…6b). Recent studies have reported that regular treadmill exercise inhibits mitochondrial accumulation of cholesterol during myocardial ischemia–reperfusion (Musman et al 2016). The heart is a metabolic omnivore, capable of utilizing fatty acids, glucose, ketone bodies, pyruvate, lactate, and amino acids (in decreasing order).…”

Section: Discussionmentioning

confidence: 99%

Untargeted metabolomics analysis of ischemia–reperfusion-injured hearts ex vivo from sedentary and exercise-trained rats

et al. 2017

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These studies shed light on novel mechanisms in which exercise-induced cardioprotection occurs in I/R that complement both the mitochondrial stabilization and antioxidant mechanisms recently described. These findings also link protein synthesis and protein degradation (protein quality control mechanisms) with exercise-linked cardioprotection and mitochondrial susceptibility for the first time in cardiac I/R.

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“…Cardenia et al ( 2017 ) observed in rat that acute exercise until exhaustion increased hepatic concentrations of 7α-OH C, 7β-OH C, 7-KC, and 27-OH C, that was prevented by 45 days of rich broccoli extract enriched-diet. On the other hand, Musman et al ( 2016 ) showed that physical training for 4 weeks reduced oxysterols in plasma and isolated mitochondria of ob/ob mice undergoing ischemia/reperfusion. This was due to the decrease of cholesterol content in the mitochondria and to the increase of the antioxidant capacity of the cardiac tissue.…”

Section: Discussionmentioning

confidence: 99%

Aerobic Exercise Training Selectively Changes Oxysterol Levels and Metabolism Reducing Cholesterol Accumulation in the Aorta of Dyslipidemic Mice

et al. 2017

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Background: Oxysterols are bioactive lipids that control cellular cholesterol synthesis, uptake, and exportation besides mediating inflammation and cytotoxicity that modulate the development of atherosclerosis. Aerobic exercise training (AET) prevents and regresses atherosclerosis by the improvement of lipid metabolism, reverse cholesterol transport (RCT) and antioxidant defenses in the arterial wall. We investigated in dyslipidemic mice the role of a 6-week AET program in the content of plasma and aortic arch cholesterol and oxysterols, the expression of genes related to cholesterol flux and the effect of the exercise-mimetic AICAR, an AMPK activator, in macrophage oxysterols concentration.Methods: Sixteen-week old male apo E KO mice fed a chow diet were included in the protocol. Animals were trained in a treadmill running, 15 m/min, 5 days/week, for 60 min (T; n = 29). A control group was kept sedentary (S; n = 32). Plasma lipids and glucose were determined by enzymatic techniques and glucometer, respectively. Cholesterol and oxysterols in aortic arch and macrophages were measured by gas chromatography/mass spectrometry. The expression of genes involved in lipid metabolism was determined by RT-qPCR. The effect of AMPK in oxysterols metabolism was determined in J774 macrophages treated with 0.25 mM AICAR.Results: Body weight and plasma TC, TG, HDL-c, glucose, and oxysterols were similar between groups. As compared to S group, AET enhanced 7β-hydroxycholesterol (70%) and reduced cholesterol (32%) in aorta. In addition, exercise increased Cyp27a1 (54%), Cd36 (75%), Cat (70%), Prkaa1 (40%), and Prkaa2 (51%) mRNA. In macrophages, the activation of AMPK followed by incubation with HDL2 increased Abca1 (52%) and Cd36 (220%) and decrease Prkaa1 (19%), Cyp27a1 (47%) and 7α-hydroxycholesterol level.Conclusion: AET increases 7β-hydroxycholesterol in the aortic arch of dyslipidemic mice, which is related to the enhanced expression of Cd36. In addition, the increase and reduction of Cyp27a1 and Cyp7b1 in trained mice may contribute to enhance levels of 27-OH C. Both oxysterols may act as an alternative pathway for the RCT contributing to the reduction of cholesterol in the aortic arch preventing atherogenesis.

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Regular treadmill exercise inhibits mitochondrial accumulation of cholesterol and oxysterols during myocardial ischemia-reperfusion in wild-type and ob/ob mice

Cited by 24 publications

References 42 publications

Protective effects of leptin against cerebral ischemia/reperfusion injury (Review)

Protective effects of leptin against cerebral ischemia/reperfusion injury (Review)

Untargeted metabolomics analysis of ischemia–reperfusion-injured hearts ex vivo from sedentary and exercise-trained rats

Aerobic Exercise Training Selectively Changes Oxysterol Levels and Metabolism Reducing Cholesterol Accumulation in the Aorta of Dyslipidemic Mice

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