Bioactive Milk-Derived Nutrient MFG-E8 Ameliorates Skeletal Muscle Atrophy Induced by Mitochondria Damage in Aging Rat via Activating MAPK/ERK Signaling Pathway.

Kaifang Guan, Xiaolin Liu, Yuhao Mao, Yirong Mao, Ying Ma, Rongchu Wang, Qiming Li

School of Medicine and Health, Harbin Institute of Technology, Harbin 150001, Heilongjiang, China.School of Medicine and Health, Harbin Institute of Technology, Harbin 150001, Heilongjiang, China. · pubmed

Paper

Abstract

Sarcopenia is an age-related muscle loss, fiber number and decreased regenerative capacity with increased abundance of ROS levels and electron transport chain (ETC) abnormalities. The aim of the study is to investigate the anti-sarcopenia effect of MFG-E8 in alleviating skeletal muscle dysfunction induced by D-gal, reveal the mechanism on promoting myoblast cell proliferation and mediating cell cycle. In vivo experiment showed that MFG-E8 can improve the anti-oxidant status and increase soleus muscle mass (35.61%) and fiber diameter (39.72%) in the aging rats. Western Blot assay preliminarily proved that increased ERK phosphorylation determines the repairment of injured skeletal muscle, but not JNK and p38. Vitro experiments further verified that MFG-E8 can increase the number of mitochondria, cell vitality, cell density and reduce apoptosis rate. Flow cytometry and qRT-PCR proved that MFG-E8 promoted cell proliferation by upregulating mRNA expression of cyclin D1, cyclin E1, CDKs, and downregulating mRNA expression of p21 and p27, thereby increasing the S, G2/M phase and decreasing G0/G1 phase. Molecular level further proved that MFG-E8 mediated cell cycle and promoted cell proliferation by activating MAPK/ERK signaling pathway.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the effects of MFG-E8 on skeletal muscle atrophy, which is a significant aspect of sarcopenia, a condition associated with aging. By focusing on the mechanisms that promote muscle regeneration and mitigate age-related muscle loss, the research addresses a root cause of aging-related decline in physical function. However, while the findings are solid and contribute to the understanding of muscle health in aging, they do not present groundbreaking insights or transformative implications for the broader field of longevity research. Thus, the impact is rated as limited.

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