Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis
Summary: Although maternal exercise (ME) becomes increasingly uncommon, the effects of ME on offspring muscle metabolic health remain largely undefined. Maternal mice are subject to daily exercise during pregnancy, which enhances mitochondrial biogenesis during fetal muscle development; this is corr...
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| Format: | Article |
| Language: | English |
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Elsevier
2020-12-01
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| Series: | Cell Reports |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124720314509 |
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| author | Jun Seok Son Song Ah Chae Hongyang Wang Yanting Chen Alejandro Bravo Iniguez Jeanene M. de Avila Zhihua Jiang Mei-Jun Zhu Min Du |
| author_facet | Jun Seok Son Song Ah Chae Hongyang Wang Yanting Chen Alejandro Bravo Iniguez Jeanene M. de Avila Zhihua Jiang Mei-Jun Zhu Min Du |
| author_sort | Jun Seok Son |
| collection | DOAJ |
| description | Summary: Although maternal exercise (ME) becomes increasingly uncommon, the effects of ME on offspring muscle metabolic health remain largely undefined. Maternal mice are subject to daily exercise during pregnancy, which enhances mitochondrial biogenesis during fetal muscle development; this is correlated with higher mitochondrial content and oxidative muscle fibers in offspring muscle and improved endurance capacity. Apelin, an exerkine, is elevated due to ME, and maternal apelin administration mirrors the effect of ME on mitochondrial biogenesis in fetal muscle. Importantly, both ME and apelin induce DNA demethylation of the peroxisome proliferator-activated receptor γ coactivator-1α (Ppargc1a) promoter and enhance its expression and mitochondrial biogenesis in fetal muscle. Such changes in DNA methylation were maintained in offspring, with ME offspring muscle expressing higher levels of PGC-1α1/4 isoforms, explaining improved muscle function. In summary, ME enhances DNA demethylation of the Ppargc1a promoter in fetal muscle, which has positive programming effects on the exercise endurance capacity and protects offspring muscle against metabolic dysfunction. |
| first_indexed | 2024-12-14T01:53:29Z |
| format | Article |
| id | doaj.art-758618a5082f437c859d17b8228a5bf1 |
| institution | Directory Open Access Journal |
| issn | 2211-1247 |
| language | English |
| last_indexed | 2024-12-14T01:53:29Z |
| publishDate | 2020-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Cell Reports |
| spelling | doaj.art-758618a5082f437c859d17b8228a5bf12022-12-21T23:21:18ZengElsevierCell Reports2211-12472020-12-01339108461Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial BiogenesisJun Seok Son0Song Ah Chae1Hongyang Wang2Yanting Chen3Alejandro Bravo Iniguez4Jeanene M. de Avila5Zhihua Jiang6Mei-Jun Zhu7Min Du8Nutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA; School of Molecular Biosciences, Washington State University, Pullman, WA 99164, USANutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USAInstitute of Animal Husbandry and Veterinary Science, Shanghai Academy of Agricultural Sciences, Shanghai, ChinaNutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USASchool of Food Science, Washington State University, Pullman, WA 99164, USANutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USANutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USASchool of Food Science, Washington State University, Pullman, WA 99164, USANutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA; School of Molecular Biosciences, Washington State University, Pullman, WA 99164, USA; Corresponding authorSummary: Although maternal exercise (ME) becomes increasingly uncommon, the effects of ME on offspring muscle metabolic health remain largely undefined. Maternal mice are subject to daily exercise during pregnancy, which enhances mitochondrial biogenesis during fetal muscle development; this is correlated with higher mitochondrial content and oxidative muscle fibers in offspring muscle and improved endurance capacity. Apelin, an exerkine, is elevated due to ME, and maternal apelin administration mirrors the effect of ME on mitochondrial biogenesis in fetal muscle. Importantly, both ME and apelin induce DNA demethylation of the peroxisome proliferator-activated receptor γ coactivator-1α (Ppargc1a) promoter and enhance its expression and mitochondrial biogenesis in fetal muscle. Such changes in DNA methylation were maintained in offspring, with ME offspring muscle expressing higher levels of PGC-1α1/4 isoforms, explaining improved muscle function. In summary, ME enhances DNA demethylation of the Ppargc1a promoter in fetal muscle, which has positive programming effects on the exercise endurance capacity and protects offspring muscle against metabolic dysfunction.http://www.sciencedirect.com/science/article/pii/S2211124720314509fetusPGC-1αDNA methylationendurance capacitymitochondrial biogenesismaternal exercise |
| spellingShingle | Jun Seok Son Song Ah Chae Hongyang Wang Yanting Chen Alejandro Bravo Iniguez Jeanene M. de Avila Zhihua Jiang Mei-Jun Zhu Min Du Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis Cell Reports fetus PGC-1α DNA methylation endurance capacity mitochondrial biogenesis maternal exercise |
| title | Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis |
| title_full | Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis |
| title_fullStr | Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis |
| title_full_unstemmed | Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis |
| title_short | Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis |
| title_sort | maternal inactivity programs skeletal muscle dysfunction in offspring mice by attenuating apelin signaling and mitochondrial biogenesis |
| topic | fetus PGC-1α DNA methylation endurance capacity mitochondrial biogenesis maternal exercise |
| url | http://www.sciencedirect.com/science/article/pii/S2211124720314509 |
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