Disruption of skeletal muscle mitochondrial network genes and miRNAs in amyotrophic lateral sclerosis

Russell, Aaron P.; Wada, Shogo; Vergani, Lodovica; Hock, M. Benjamin; Lamon, Séverine; Léger, Bertrand; Ushida, Takashi; Cartoni, Romain; Wadley, Glenn D.; Hespel, Peter; Kralli, Anastasia; Sorarù, Gianni; Angelini, C.; Akimoto, Takayuki

doi:10.1016/j.nbd.2012.08.015

Cited by 179 publications

(176 citation statements)

References 72 publications

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“…*P < 0.05 vs. pEGP. a reduction in PGC-1a and mitochondrial biogenesis and function in skeletal muscle (33). Similarly, endurance exercise downregulates miR-23 levels and upregulates PGC-1a, along with several downstream targets of PGC1a, including aminolevulinate synthase, CS, and Cyt C mRNAs (32).…”

Section: Discussionmentioning

confidence: 99%

“…This suggests that inhibition of PARP activities is beneficial to promote skeletal muscle energy expenditure. One promising strategy to inhibit the activity of endogenous PARPs would be modulation of the miRNA-mediated pathway, which plays a key role in skeletal muscle metabolism (22,(29)(30)(31)(32)(33). To achieve this, we attempted to identify miRNAs that control PARP expression.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-149 Inhibits PARP-2 and Promotes Mitochondrial Biogenesis via SIRT-1/PGC-1α Network in Skeletal Muscle

et al. 2014

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High-fat diet (HFD) plays a central role in the initiation of mitochondrial dysfunction that significantly contributes to skeletal muscle metabolic disorders in obesity. However, the mechanism by which HFD weakens skeletal muscle metabolism by altering mitochondrial function and biogenesis is unknown. Given the emerging roles of microRNAs (miRNAs) in the regulation of skeletal muscle metabolism, we sought to determine whether activation of a specific miRNA pathway would rescue the HFD-induced mitochondrial dysfunction via the sirtuin-1 (SIRT-1)/ peroxisome proliferator–activated receptor γ coactivator-1α (PGC-1α) pathway, a pathway that governs genes necessary for mitochondrial function. We here report that miR-149 strongly controls SIRT-1 expression and activity. Interestingly, miR-149 inhibits poly(ADP-ribose) polymerase-2 (PARP-2) and so increased cellular NAD+ levels and SIRT-1 activity that subsequently increases mitochondrial function and biogenesis via PGC-1α activation. In addition, skeletal muscles from HFD-fed obese mice exhibit low levels of miR-149 and high levels of PARP-2, and they show reduced mitochondrial function and biogenesis due to a decreased activation of the SIRT-1/PGC-1α pathway, suggesting that mitochondrial dysfunction in the skeletal muscle of obese mice may be because of, at least in part, miR-149 dysregulation. Overall, miR-149 may be therapeutically useful for treating HFD-induced skeletal muscle metabolic disorders in such pathophysiological conditions as obesity and type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MicroRNA-149 Inhibits PARP-2 and Promotes Mitochondrial Biogenesis via SIRT-1/PGC-1α Network in Skeletal Muscle

et al. 2014

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“…Muscle Biopsies-Human skeletal muscle samples were from the belly of the vastus lateralis muscle and have been described previously (24,41).…”

Section: Methodsmentioning

confidence: 99%

“…ute to the pathology of these states (21)(22)(23)(24). Supporting this notion, transgenic expression of PGC-1␣ in skeletal muscle protects from age-related or denervation-induced muscle atrophy and delays the onset of mitochondrial myopathies, whereas transgenic expression of PGC-1␤ in the heart protects from sepsis-induced cardiomyopathy (23,(25)(26)(27).…”

mentioning

confidence: 92%

Peroxisome Proliferator-activated Receptor γ Coactivator 1 (PGC-1)- and Estrogen-related Receptor (ERR)-induced Regulator in Muscle 1 (PERM1) Is a Tissue-specific Regulator of Oxidative Capacity in Skeletal Muscle Cells

Cho

Hazen

Russell

et al. 2013

Journal of Biological Chemistry

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105

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Background:The regulatory mechanisms that control skeletal muscle bioenergetics are not fully understood. Results: The muscle-specific protein Perm1 is induced by exercise and exercise-activated regulators and controls the expression of energy homeostasis genes. Conclusion: Perm1 is a regulator of mitochondrial oxidative capacity and bioenergetics. Significance: Novel muscle regulators of bioenergetics may facilitate approaches for preserving/enhancing muscle function.

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“…PGC1A, which encodes the transcriptional cofactor peroxisome proliferator-activated receptor-␥ coactivator-1␣, is an established inducer of mitochondrial ␤-oxidation and electron transport and is a direct target of miR-23a (44). Furthermore, miR-23a regulates glucose transport (34) and interferes with mitochondrial function (37). Interestingly, we have previously shown that CC is associated with increased expression of genes (cytochrome c oxidase subunit 8A, cytochrome b5 type A, cytochrome c-1, pyruvate carboxylase, branched-chain aminotransferase) related to energy expenditure in human adipose tissue (11).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA profiling links miR-378 to enhanced adipocyte lipolysis in human cancer cachexia

Kulyté

Lorente‐Cebrián

Gao

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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Cancer cachexia is associated with pronounced adipose tissue loss due to, at least in part, increased fat cell lipolysis. MicroRNAs (miRNAs) have recently been implicated in controlling several aspects of adipocyte function. To gain insight into the possible impact of miRNAs on adipose lipolysis in cancer cachexia, global miRNA expression was explored in abdominal subcutaneous adipose tissue from gastrointestinal cancer patients with ( n = 10) or without ( n = 11) cachexia. Effects of miRNA overexpression or inhibition on lipolysis were determined in human in vitro differentiated adipocytes. Out of 116 miRNAs present in adipose tissue, five displayed distinct cachexia-associated expression according to both microarray and RT-qPCR. Four (miR-483–5p/-23a/-744/-99b) were downregulated, whereas one (miR-378) was significantly upregulated in cachexia. Adipose expression of miR-378 associated strongly and positively with catecholamine-stimulated lipolysis in adipocytes. This correlation is most probably causal because overexpression of miR-378 in human adipocytes increased catecholamine-stimulated lipolysis. In addition, inhibition of miR-378 expression attenuated stimulated lipolysis and reduced the expression of LIPE, PLIN1, and PNPLA2, a set of genes encoding key lipolytic regulators. Taken together, increased miR-378 expression could play an etiological role in cancer cachexia-associated adipose tissue loss via effects on adipocyte lipolysis.

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Disruption of skeletal muscle mitochondrial network genes and miRNAs in amyotrophic lateral sclerosis

Cited by 179 publications

References 72 publications

MicroRNA-149 Inhibits PARP-2 and Promotes Mitochondrial Biogenesis via SIRT-1/PGC-1α Network in Skeletal Muscle

MicroRNA-149 Inhibits PARP-2 and Promotes Mitochondrial Biogenesis via SIRT-1/PGC-1α Network in Skeletal Muscle

Peroxisome Proliferator-activated Receptor γ Coactivator 1 (PGC-1)- and Estrogen-related Receptor (ERR)-induced Regulator in Muscle 1 (PERM1) Is a Tissue-specific Regulator of Oxidative Capacity in Skeletal Muscle Cells

MicroRNA profiling links miR-378 to enhanced adipocyte lipolysis in human cancer cachexia

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