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Milk fat globule membrane protein promotes C2C12 cell proliferation through the PI3K/Akt signaling pathway

  • He Li
    ,
  • Weili Xu
    ,
  • Ying Ma
    ,
  • Shaobo Zhou
    ,
  • Ran Xiao
Research Output: Contribution to journal Article Peer-review

Open access

Abstract

Milk fat globule membrane (MFGM) protein is known to have several health benefits, including an anti-sarcopenia effect; however, its mechanism is unclear. The aim of this study was to investigate the potential mechanism of action of the MFGM protein. The MFGM protein was extracted and separated into 4 fractions, and Fraction 2 (57 % of total MFGM) demonstrated the greatest effect on C2C12 cell proliferation. Milk fat globule-EGF factor 8 (MFG-E8) accounted for 82.35 % of the MFGM protein. The effects of whole Fraction 2 (100 μg/mL, 200 μg/mL and 300 μg/mL) on cell proliferation and morphology were measured. Using qRT-PCR or a Western blot assay, several regulatory factors, e.g., PI3K P85α, p-pI3K p85α (Tyr 508), Akt, p-Akt (Ser 473), mTOR and p-mTOR (Ser 2448), were measured in cells incubated with 200 μg/mL of Fraction 2 with or without wortmannin. The results demonstrated that Fraction 2 induced C2C12 cell proliferation in a dose-dependent manner, upregulated the mRNA expression of mTOR and p70S6K, and activated PI3K, Akt, mTOR and P70S6K phosphorylation; however, Fraction 2 inhibited FOXO3a and 4E-BP. The results demonstrate that the MFGM protein, predominantly MFG-E8, promotes cell proliferation through the PI3K/Akt/mTOR signaling pathway. This study elucidated the molecular mechanism of the MFGM protein, primarily MFG-E8, in promoting C2C12 cell proliferation via the PI3K/Akt/mTOR/P70S6K signal pathway.

Publication Information

Output type

Research Output: Contribution to journal Article Peer-review

Original language

English

Pages from-to (Number of pages)

Pages 1305-1314

Journal (Volume, Issue Number)

International Journal of Biological Macromolecules (Volume 114, Issue July)

Publication milestones

  • Accepted/In press - 05/04/2018
  • Published - 07/04/2018

Publication status

Published - 07/04/2018

ISSN

0141-8130

External Publication IDs

  • handle.net: 10547/622670
  • Scopus: 85045392591