Exercise-Induced Changes in Caveolin-1, Depletion of Mitochondrial Cholesterol, and the Inhibition of Mitochondrial Swelling in Rat Skeletal Muscle but Not in the Liver

Flis, Damian Józef; Olek, Robert A.; Kaczor, Jan Jacek; Rodziewicz, Ewa; Halon, Malgorzata; Antosiewicz, Jędrzej; Woźniak, Michał; Gabbianelli, Rosita; Ziółkowski, Wiesław

doi:10.1155/2016/3620929

Cited by 8 publications

(10 citation statements)

References 38 publications

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“…However, there was an opposite trend in liver from Tg -/- mice, with a significant increase for complexes III and IV activities. This particular response could be explained by the specific effect of physiological stresses on the mitochondrial metabolism in various tissues and specifically the liver [35,36]. …”

Section: Resultsmentioning

confidence: 99%

“…Mitochondrial metabolism is indeed affected in Tg -/- mice, with a marked decrease in complexes I, III, IV activities in brain and muscle, and an increase in complexes III and IV activities in liver. This discrepancy is not unlikely, given the specificity of each tissue and each cell type in the response to physiological stresses [35,36] or to mutations [55,56]. …”

Section: Discussionmentioning

confidence: 99%

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Bovine and murine models highlight novel roles for SLC25A46 in mitochondrial dynamics and metabolism, with implications for human and animal health

et al. 2017

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Neuropathies are neurodegenerative diseases affecting humans and other mammals. Many genetic causes have been identified so far, including mutations of genes encoding proteins involved in mitochondrial dynamics. Recently, the “Turning calves syndrome”, a novel sensorimotor polyneuropathy was described in the French Rouge-des-Prés cattle breed. In the present study, we determined that this hereditary disease resulted from a single nucleotide substitution in SLC25A46, a gene encoding a protein of the mitochondrial carrier family. This mutation caused an apparent damaging amino-acid substitution. To better understand the function of this protein, we knocked out the Slc25a46 gene in a mouse model. This alteration affected not only the nervous system but also altered general metabolism, resulting in premature mortality. Based on optic microscopy examination, electron microscopy and on biochemical, metabolic and proteomic analyses, we showed that the Slc25a46 disruption caused a fusion/fission imbalance and an abnormal mitochondrial architecture that disturbed mitochondrial metabolism. These data extended the range of phenotypes associated with Slc25a46 dysfunction. Moreover, this Slc25a46 knock-out mouse model should be useful to further elucidate the role of SLC25A46 in mitochondrial dynamics.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Bovine and murine models highlight novel roles for SLC25A46 in mitochondrial dynamics and metabolism, with implications for human and animal health

et al. 2017

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“…Our findings imply that the reduction in cholesterol contents, improvement in bioenergetics, and attenuation of oxidative stress may be a result of an increase in the Cav-1 protein level in the crude mitochondria of the skeletal muscle in trained ALS mice. As we previously indicated, these changes might be related to a dynamic physiological process that may help mitochondria adapt to stress conditions [ 15 , 22 , 34 ].…”

Section: Discussionmentioning

confidence: 99%

“…First, the Cav-1 protein plays a critical role as a modifier of mitochondrial respiratory chain function, the antioxidant enzyme defense system, and mitochondrial biogenesis under oxidative stress conditions [ 37 ]. Second, the increase in the Cav-1 protein that resulted in lowering the cholesterol content in the crude mitochondrial fraction seems to play a main role in exercise-induced mitoprotection via remodeling of MAMs [ 15 , 22 ].…”

Section: Discussionmentioning

confidence: 99%

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Swim Training Modulates Skeletal Muscle Energy Metabolism, Oxidative Stress, and Mitochondrial Cholesterol Content in Amyotrophic Lateral Sclerosis Mice

Flis

Dzik

Kaczor

et al. 2018

Oxidative Medicine and Cellular Longevity

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Recently, in terms of amyotrophic lateral sclerosis (ALS), much attention has been paid to the cell structures formed by the mitochondria and the endoplasmic reticulum membranes (MAMs) that are involved in the regulation of Ca2+ signaling, mitochondrial bioenergetics, apoptosis, and oxidative stress. We assumed that remodeling of these structures via swim training may accompany the prolongation of the ALS lifespan. In the present study, we used transgenic mice with the G93A hmSOD1 gene mutation. We examined muscle energy metabolism, oxidative stress parameters, and markers of MAMs (Caveolin-1 protein level and cholesterol content in crude mitochondrial fraction) in groups of mice divided according to disease progression and training status. The progression of ALS was related to the lowering of Caveolin-1 protein levels and the accumulation of cholesterol in a crude mitochondrial fraction. These changes were associated with aerobic and anaerobic energy metabolism dysfunction and higher oxidative stress. Our data indicated that swim training prolonged the lifespan of ALS mice with accompanying changes in MAM components. Swim training also maintained mitochondrial function and lowered oxidative stress. These data suggest that modification of MAMs might play a crucial role in the exercise-induced deceleration of ALS development.

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Combined exercise and calorie restriction therapies restore contractile and mitochondrial functions in skeletal muscle of obese–insulin resistant rats

Pattanakuhar

Sutham²,

Sripetchwandee³

et al. 2019

Nutrition

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Exercise-Induced Changes in Caveolin-1, Depletion of Mitochondrial Cholesterol, and the Inhibition of Mitochondrial Swelling in Rat Skeletal Muscle but Not in the Liver

Cited by 8 publications

References 38 publications

Bovine and murine models highlight novel roles for SLC25A46 in mitochondrial dynamics and metabolism, with implications for human and animal health

Bovine and murine models highlight novel roles for SLC25A46 in mitochondrial dynamics and metabolism, with implications for human and animal health

Swim Training Modulates Skeletal Muscle Energy Metabolism, Oxidative Stress, and Mitochondrial Cholesterol Content in Amyotrophic Lateral Sclerosis Mice

Combined exercise and calorie restriction therapies restore contractile and mitochondrial functions in skeletal muscle of obese–insulin resistant rats

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