MicroRNA-494 regulates mitochondrial biogenesis in skeletal muscle through mitochondrial transcription factor A and Forkhead box j3

Yamamoto, Hirotaka; Morino, Katsutaro; Nishio, Yoshihiko; Ugi, Satoshi; Yoshizaki, Takeshi; Kashiwagi, Atsunori; Maegawa, Hiroshi

doi:10.1152/ajpendo.00097.2012

Cited by 116 publications

(94 citation statements)

References 36 publications

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“…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%

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%

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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“…Because this slow-twitch muscle does not express DLK1, we predict that this phenotype may be influenced by other miRs within this cluster through an unknown mechanism. Among the miRs, miR-411 regulates myogenesis by targeting myogenic factors (39), and miR-494 regulates the mitochondrial biogenesis of skeletal muscle by targeting mitochondrial transcription factor A and Forkhead box j3 (40). MiR-329 can inhibit cell proliferation and angiogenesis in vitro by targeting E2F and KDM1A (41,42).…”

Section: Discussionmentioning

confidence: 99%

Regulation of DLK1 by the maternally expressed miR-379/miR-544 cluster may underlie callipyge polar overdominance inheritance

Gao

Chen

Wang

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Inheritance of the callipyge phenotype in sheep is an example of polar overdominance inheritance, an unusual mode of inheritance. To investigate the underlying molecular mechanism, we profiled the expression of the genes located in the Delta-like 1 homolog (Dlk1)-type III iodothyronine deiodinase (Dio3) imprinting region in mice. We found that the transcripts of the microRNA (miR) 379/miR-544 cluster were highly expressed in neonatal muscle and paralleled the expression of the Dlk1. We then determined the in vivo role of the miR-379/miR-544 cluster by establishing a mouse line in which the cluster was ablated. The maternal heterozygotes of young mutant mice displayed a hypertrophic tibialis anterior muscle, extensor digitorum longus muscle, gastrocnemius muscle, and gluteus maximus muscle and elevated expression of the DLK1 protein. Reduced expression of DLK1 was mediated by miR-329, a member of this cluster. Our results suggest that maternal expression of the imprinted miR-379/miR-544 cluster regulates paternal expression of the Dlk1 gene in mice. We therefore propose a miR-based molecular working model for polar overdominance inheritance. muscle hypertrophy | callipyge | DLK1 | miR-379/miR-544 cluster T he callipyge (CLPG) phenotype can be characterized by an increase in muscle mass due to muscular hypertrophy and a unique non-Mendelian mode of inheritance (1-3). CLPG individuals are born with normal muscle histology and develop muscle hypertrophy at ∼1 mo of age. This hypertrophy occurs primarily in the muscles of the pelvic limbs and loin and some muscles in the shoulder, which are enriched with a high proportion of type IIB fast-twitch glycolytic fibers (4). Although the molecular regulation of these hypertrophic processes is yet to be determined, Delta-like 1 homolog (DLK1) is found to be the causative protein (5-10). The unique mode of inheritance of the CLPG phenotype has attracted a great deal of attention within the scientific community. The CLPG offspring inherit the phenotype only when the mutated allele comes from the father and the wild-type allele from the mother (CLPG PAT /+ MAT ). CLPG PAT /CLPG MAT offspring exhibit a wild-type phenotype, despite carrying a CLPG mutation on the paternal chromosome. This unusual mode of inheritance led to the development of the genetic concept of polar overdominance (2, 11).The CLPG mutation has been mapped to the Dlk1-Dio3 imprinted domain, which spans ∼1 Mb and harbors at least three protein-encoding genes, including Dlk1, Peg11/Rtl1, and Dio3, and multiple noncoding RNA genes, including Gtl2, anti-Peg11/anti-Rtl1, Meg8, Mirg, C/D small nucleolar RNAs (snoRNAs), and microRNA clusters [the microRNA (miR) 379 and miR-127 clusters] (12-14). The coding genes are expressed paternally, whereas the noncoding genes are expressed maternally (15,16). Further analysis revealed a point mutation (A to G transition) within the intergenic region between the Dlk1 and Gtl2 genes of the imprinted Dlk1-Dio3 region (17, 18), which affects a muscle-specific, long-range cis-acting ...

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“…Concomitant activation of AMP/AMPK pathway, Ca ++ /CaMK and PDK pathways has been related to the decrease in class IIa HDAC activity, resulting in hypomethylation and consequent increase in expression of PGC-1α, PPAR-γ and MEF-2, factors associated to expressions of GLUT-4 and mitochondrial genes [87,88]. The activities of MRFs, including MyoD-1, myogenin, MEF-2, SRF and MRTF-A, are also associated to miR expression, such as miR-31, miR-34c, miR-181, miR-206, miR-223, miR-335, miR-449, and, miR-494 [89,90].…”

Section: Physical Exercise and Gene Expressionmentioning

confidence: 99%

“…These mechanisms modulate, positively or negatively, expressions of the genes related to different exercise-induced adaptative processes such as: proliferation of precursor cells and differentiation of microtubules, mass maintenance and/or muscle hypertrophy, determination of muscle fiber type, mitochondrial biogenesis and oxidative capacity, and muscle contractility. Aerobic physical exercise negatively modulates expression of various miRs involved in the processes presented above, such as miR-1, miR-26a, miR-29a, miR-378, miR-125a, miR-183, miR-189, miR-432, miR-494, miR-575, miR-616, miR-637, miR-696, and miR-761 [1,51,84,85,89,92,93].…”

Section: Physical Exercise and Gene Expressionmentioning

confidence: 99%

Regulation of Gene Expression by Exercise-Related Micrornas

Masi¹,

Serdan²,

Levada‐Pires³

et al. 2016

Cell Physiol Biochem

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Gene expression control by microRNAs (miRs) is an important mechanism for maintenance of cellular homeostasis in physiological and pathological conditions as well as in response to different stimuli including nutritional factors and exercise. MiRs are involved in regulation of several processes such as growth and development, fuel metabolism, insulin secretion, immune function, miocardium remodeling, cell proliferation, differenciation, survival, and death. These molecules have also been proposed to be potential biomarkers and/or therapeutical targets in obesity, type 2 diabetes mellitus, cardiovascular diseases, metabolic syndrome, and cancer. MiRs are released by most cells and potentially act on intercellular communication to borderer or distant cells. Various studies have been performed to elucidate the involvement of miRs in exercise-induced effects. The aims of this review are: 1) to bring up the main advances for the comprehension of the mechanisms of action of miRs; 2) to present the main results on miR involvement in physical exercise; 3) to discuss the physiological effects of miRs modified by exercise. The state of the art and the perspectives on miRs associated with physical exercise will be presented. Thus, this review is important for updating recent advances and driving further strategies and studies on the exercise-related miR research.

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MicroRNA-494 regulates mitochondrial biogenesis in skeletal muscle through mitochondrial transcription factor A and Forkhead box j3

Abstract: Kashiwagi A, Maegawa H. MicroRNA-494 regulates mitochondrial biogenesis in skeletal muscle through mitochondrial transcription factor A and Forkhead box j3.

Cited by 116 publications

References 36 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

Regulation of DLK1 by the maternally expressed miR-379/miR-544 cluster may underlie callipyge polar overdominance inheritance

Regulation of Gene Expression by Exercise-Related Micrornas

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