Lactoferrin promotes murine C2C12 myoblast proliferation and differentiation and myotube hypertrophy
Kitakaze T., Oshimo M., Kobayashi Y., Ryu M., Suzuki YA., Inui H.
Animal Study, published in Mol Med Rep (2018) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Mol Med Rep (2018)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 29436684
- PMCID
- PMC5866037
- DOI
- 10.3892/mmr.2018.8603
- Citations
- 13
Abstract (original English)
Lactoferrin (Lf) is a multifunctional glycoprotein, which promotes the proliferation of murine C2C12 myoblasts. In the present study, it was investigated how Lf promotes myoblast proliferation and whether Lf promotes myoblast differentiation or induces myotube hypertrophy. Lf promoted the proliferation of myoblasts in a dose‑dependent manner. Myoblast proliferation increased on day 3 when myoblasts were cultured in the presence of Lf for three days and also when myoblasts were cultured in the presence of Lf for the first day and in the absence of Lf for the subsequent two days. In addition, Lf induced the phosphorylation of extracellular signal‑regulated kinase (ERK)1/2 in myoblasts. The mitogen‑activated protein kinase kinase 1/2 inhibitor U0126 inhibited Lf‑induced ERK1/2 phosphorylation and repressed Lf‑promoted myoblast proliferation. C2C12 myoblasts, myotubes and skeletal muscle expressed low‑density lipoprotein receptor‑related protein (LRP)1 mRNA and Lf‑promoted myoblast proliferation was attenuated by an LRP1 antagonist or LRP1 gene silencing. The knockdown of LRP1 repressed Lf‑induced phosphorylation of ERK1/2. Furthermore, when myoblasts were induced to differentiate, Lf increased the expression of the myotube‑specific structural protein, myosin heavy chain (MyHC) and promoted myotube formation. Knockdown of LRP1 repressed Lf‑induced MyHC expression. Lf also increased
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.