Prevention of Disuse Muscle Atrophy by Dietary Ingestion of 8-Prenylnaringenin in Denervated Mice

Mukai, Rie; Horikawa, Hitomi; Fujikura, Yutaka; Kawamura, Tomoyuki; Nemoto, Hisao; Nikawa, Takeshi; Terao, Junji

doi:10.1371/journal.pone.0045048

Cited by 76 publications

(95 citation statements)

References 48 publications

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“…Prenylation was thought to elevate bioactivity by altering hydrophobicity, thus enhancing cellular uptake. Recently, however, bioactivity was thought to be enhanced by possible interactions between prenylated polyphenols and target proteins (Neal and Wu, 1994;Adams et al, 2006;Mukai et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Molecular Cloning and Characterization of a Geranyl Diphosphate-Specific Aromatic Prenyltransferase from Lemon

Munakata¹,

Inoue

Koeduka

et al. 2014

Plant Physiology

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Prenyl residues confer divergent biological activities such as antipathogenic and antiherbivorous activities on phenolic compounds, including flavonoids, coumarins, and xanthones. To date, about 1,000 prenylated phenolics have been isolated, with these compounds containing various prenyl residues. However, all currently described plant prenyltransferases (PTs) have been shown specific for dimethylallyl diphosphate as the prenyl donor, while most of the complementary DNAs encoding these genes have been isolated from the Leguminosae. In this study, we describe the identification of a novel PT gene from lemon (Citrus limon), ClPT1, belonging to the homogentisate PT family. This gene encodes a PT that differs from other known PTs, including flavonoid-specific PTs, in polypeptide sequence. This membrane-bound enzyme was specific for geranyl diphosphate as the prenyl donor and coumarin as the prenyl acceptor. Moreover, the gene product was targeted to plastid in plant cells. To our knowledge, this is the novel aromatic PT specific to geranyl diphosphate from citrus species.

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Section: Discussionmentioning

confidence: 99%

Molecular Cloning and Characterization of a Geranyl Diphosphate-Specific Aromatic Prenyltransferase from Lemon

Munakata¹,

Inoue

Koeduka

et al. 2014

Plant Physiology

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“…Previously, periodic injection of the flavonol-type flavonoid quercetin into the gastrocnemius muscle was shown to be effective in preventing muscle weight loss in mice that underwent tail suspension (11). Furthermore, the principal flavonoid prenylation enabled naringenin, which is commonly found in grapefruit and sour oranges, to prevent muscle atrophy induced by disuse in denervated mice (13). In addition, flavonoids prevent muscle atrophy induced by inflammatory conditions such as sepsis.…”

mentioning

confidence: 99%

Flavones Inhibit LPS-Induced Atrogin-1/MAFbx Expression in Mouse C2C12 Skeletal Myotubes

Shiota

Abe

Kawai

et al. 2015

J Nutr Sci Vitaminol

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Summary Muscle atrophy is a complex process that occurs as a consequence of various stress events. Muscle atrophy-associated genes (atrogenes) such as atrogin-1/MAFbx and MuRF-1 are induced early in the atrophy process, and the increase in their expression precedes the loss of muscle weight. Although antioxidative nutrients suppress atrogene expression in skeletal muscle cells, the inhibitory effects of flavonoids on inflammation-induced atrogin-1/MAFbx expression have not been clarified. Here, we investigated the inhibitory effects of flavonoids on lipopolysaccharide (LPS)-induced atrogin-1/MAFbx expression. We examined whether nine flavonoids belonging to six flavonoid categories inhibited atrogin-1/ MAFbx expression in mouse C2C12 myotubes. Two major flavones, apigenin and luteolin, displayed potent inhibitory effects on atrogin-1/MAFbx expression. The pretreatment with apigenin and luteolin significantly prevented the decrease in C2C12 myotube diameter caused by LPS stimulation. Importantly, the pretreatment of LPS-stimulated myoblasts with these flavones significantly inhibited LPS-induced JNK phosphorylation in C2C12 myotubes, resulting in the significant suppression of atrogin-1/MAFbx promoter activity. These results suggest that apigenin and luteolin, prevent LPS-mediated atrogin-1/MAFbx expression through the inhibition of the JNK signaling pathway in C2C12 myotubes. Thus, these flavones, apigenin and luteolin, may be promising agents to prevent LPS-induced muscle atrophy.

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“…In line with these results, the intake of prenylated metabolite of Nar (8-prenyl naringenin), full agonist on ERa and pronounced antagonist on ERb (Roelens et al 2006), accelerates AKT phosphorylation preventing muscle atrophy, promoting post-natal growth, and delaying the degradation of skeletal muscles in denervated mice (Mukai et al 2012). Intriguingly, no effect was reported by Nar intake on AKT activation and muscle recovery in the same mice (Mukai et al 2012).…”

Section: Discussionmentioning

confidence: 58%

Naringenin modulates skeletal muscle differentiation via estrogen receptor α and β signal pathway regulation

et al. 2014

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Several experiments sustain healthful benefits of the flavanone naringenin (Nar) against chronic diseases including its protective effects against estrogen-related cancers. These experiments encourage Nar use in replacing estrogen treatment in post-menopausal women avoiding the serious side effects ascribed to this hormone. However, at the present, scarce data are available on the impact of Nar on E2-regulated cell functions. This study was aimed at determining the impact of Nar on the estrogen receptor (ERa and b)-dependent signals important for 17b-estradiol (E2) effect in muscle cells (rat L6 myoblasts, mouse C2C12 myoblasts, and mouse skeletal muscle satellite cells). Dietary relevant concentration of Nar delays the appearance of skeletal muscle differentiation markers (i.e., GLUT4 translocation, myogenin, and both fetal and slow MHC isoforms) and impairs E2 effects specifically hampering ERa ability to activate AKT. Intriguingly, Nar effects are specific for E2-initiating signals because IGF-Iinduced AKT activation, and myoblast differentiation markers were not affected by Nar treatment. Only 7 days after Nar stimulation, early myoblast differentiation markers (i.e., myogenin, and fetal MHC) start to be accumulated in myoblasts. On the other hand, Nar stimulation activates, via ERb, the phosphorylation of p38/MAPK involved in reducing the reactive oxygen species formation in skeletal muscle cells. As a whole, data reported here strongly sustain that although Nar action mechanisms include the impairment of ERa signals which drive muscle cells to differentiation, the effects triggered by Nar in the presence of ERb could balance this negative effect avoiding the toxic effects produced by oxidative stress.

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Prevention of Disuse Muscle Atrophy by Dietary Ingestion of 8-Prenylnaringenin in Denervated Mice

Cited by 76 publications

References 48 publications

Molecular Cloning and Characterization of a Geranyl Diphosphate-Specific Aromatic Prenyltransferase from Lemon

Molecular Cloning and Characterization of a Geranyl Diphosphate-Specific Aromatic Prenyltransferase from Lemon

Flavones Inhibit LPS-Induced Atrogin-1/MAFbx Expression in Mouse C2C12 Skeletal Myotubes

Naringenin modulates skeletal muscle differentiation via estrogen receptor α and β signal pathway regulation

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