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Pyropia yezoensis peptide PYP1?5 protects against dexamethasone?induced muscle atrophy through the downregulation of atrogin1/MAFbx and MuRF1 in mouse C2C12 myotubes.

ABSTRACT: Skeletal muscle atrophy refers to the decline in muscle mass and strength that occurs under various conditions, including aging, starvation, cancer and other cachectic diseases. Muscle atrophy caused by aging, known as sarcopenia, primarily occurs after 50 years of age. Muscle atrophy?related genes, including atrogin1/muscle atrophy F?box (MAFbx) and muscle RING finger 1 (MuRF1), are expressed early in the muscle atrophy process, and their expression precedes the loss of muscle mass. The present study investigated the potential anti?atrophic effects of the Pyropia yezoensis peptide PYP1?5. The MTS assay did not detect cytotoxic effects of PYP1?5 on C2C12 mouse myoblast cells. Subsequently, the anti?atrophic effects of PYP1?5 on skeletal muscle cells was examined by treating C2C12 myotubes with 100 µM dexamethasone (DEX) and/or 500 ng/ml PYP1?5 for 24 h. Compared with the control, myotube diameter was reduced in DEX?treated cells, whereas PYP1?5 treatment protected against DEX?induced muscle atrophy. MAFbx and MuRF1 protein and mRNA expression levels were detected by western blot analysis and reverse transcription?quantitative polymerase chain reaction, respectively. The results demonstrated that PYP1?5 significantly reduced the expression of atrogin1/MAFbx and MuRF1. Therefore, data from the present study suggest that PYP1?5 inhibits the expression of atrogin1/MAFbx and MuRF1 in C2C12 cells, and these characteristics may be of value in the development of anti?atrophy functional foods.

SUBMITTER: Lee MK

PROVIDER: S-EPMC5436292 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature

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Pyropia yezoensis peptide PYP1‑5 protects against dexamethasone‑induced muscle atrophy through the downregulation of atrogin1/MAFbx and MuRF1 in mouse C2C12 myotubes.

Lee Min-Kyeong MK Kim Young-Min YM Kim In-Hye IH Choi Youn-Hee YH Nam Taek-Jeong TJ

Molecular medicine reports 20170407 6

Skeletal muscle atrophy refers to the decline in muscle mass and strength that occurs under various conditions, including aging, starvation, cancer and other cachectic diseases. Muscle atrophy caused by aging, known as sarcopenia, primarily occurs after 50 years of age. Muscle atrophy‑related genes, including atrogin1/muscle atrophy F‑box (MAFbx) and muscle RING finger 1 (MuRF1), are expressed early in the muscle atrophy process, and their expression precedes the loss of muscle mass. The present ...[more]

PMID: 28393223

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Project description:UnlabelledBackgroundThe p38 mitogen-activated protein kinases (MAPK) family plays pivotal roles in skeletal muscle metabolism. Recent evidence revealed that p38? and p38? exert paradoxical effects on muscle protein homeostasis. However, it is unknown why p38?, but not p38?, is capable of mediating muscle catabolism via selective activation of the C/EBP? that upregulates atrogin1/MAFbx.MethodsTryptic phosphopeptide mapping was carried out to identify p38?- and p38?-mediated phosphorylation sites in C/EBP?. Chromosome immunoprecipitation (ChIP) assay was used to evaluate p38? and p38? effect on C/EBP? binding to the atrogin1/MAFbx promoter. Overexpression or siRNA-mediated gene knockdown of p38? and p38?, and site-directed mutagenesis or knockout of C/EBP?, were used to analyze the roles of these kinases in muscle catabolism in C2C12 myotubes and mice.ResultsCellular expression of constitutively active p38? or p38? resulted in phosphorylation of C/EBP? at multiple serine and threonine residues; however, only p38? phosphorylated Thr-188, which had been known to be critical to the DNA-binding activity of C/EBP?. Only p38?, but not p38?, activated C/EBP?-binding to the atrogin1/MAFbx promoter. A C/EBP? mutant in which Thr-188 was replaced by alanine acted as a dominant-negative inhibitor of atrogin1/MAFbx upregulation induced by either p38? or Lewis lung carcinoma (LLC) cell-conditioned medium (LCM). In addition, knockdown of p38? specifically inhibited C/EBP? activation and atrogin1/MAFbx upregulation induced by LCM. Finally, expression of active p38? in mouse tibialis anterior specifically induced C/EBP? phosphorylation at Thr-188, atrogin1/MAFbx upregulation and muscle mass loss, which were blocked in C/EBP?-null mice.ConclusionsThe ? and ? isoforms of p38 MAPK are capable of recognizing distinct phosphorylation sites in a substrate. The unique capacity of p38? in mediating muscle catabolism is due to its capability in phosphorylating Thr-188 of C/EBP?.

Dataset Information

Pyropia yezoensis peptide PYP1?5 protects against dexamethasone?induced muscle atrophy through the downregulation of atrogin1/MAFbx and MuRF1 in mouse C2C12 myotubes.

Publications

Pyropia yezoensis peptide PYP1‑5 protects against dexamethasone‑induced muscle atrophy through the downregulation of atrogin1/MAFbx and MuRF1 in mouse C2C12 myotubes.

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