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Isolation of Human Myoblasts, Assessment of Myogenic Differentiation, and Store-operated Calcium Entry Measurement
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LIF is a contraction-induced myokine stimulating human myocyte proliferation

Christa Broholm1, Matthew J Laye, Claus Brandt

  • 1Rigshospitalet, Centre of Inflammation and Metabolism (CIM) 7641, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. christa.broholm@gmail.com

Journal of Applied Physiology (Bethesda, Md. : 1985)
|April 30, 2011
PubMed

Insights

Leukemia inhibitory factor (LIF) is a muscle-derived cytokine that promotes satellite cell proliferation following resistance exercise. LIF acts locally, not systemically, to regulate muscle growth and repair.

Area of Science:

  • Exercise Physiology
  • Molecular Biology
  • Muscle Biology

Background:

  • Skeletal muscle releases cytokines, known as myokines, in response to exercise.
  • Leukemia inhibitory factor (LIF) is a cytokine expressed by skeletal muscle that stimulates myoblast proliferation.

Purpose of the Study:

  • To investigate whether LIF is a contraction-induced myokine that promotes human muscle satellite cell proliferation.
  • To explore the regulatory pathways and downstream targets of LIF in muscle.

Main Methods:

  • Assessed LIF mRNA and protein expression in human skeletal muscle post-resistance exercise.
  • Examined LIF production and regulation in electrically stimulated cultured human myotubes.
  • Investigated the role of PI3K, Akt, and mTOR signaling in LIF regulation.
  • Studied the effect of exogenous LIF and LIF receptor knockdown on myoblast proliferation.
  • Analyzed the induction of transcription factors JunB and c-Myc by LIF.

Main Results:

  • Resistance exercise significantly increased LIF mRNA in skeletal muscle, but not plasma LIF levels.
  • Cultured human myotubes produced and secreted LIF upon electrical stimulation, indicating local action.
  • PI3K, Akt, and mTOR signaling pathways were involved in regulating LIF expression.
  • Exogenous LIF enhanced human myoblast proliferation, while LIF receptor knockdown inhibited it.
  • LIF induced the proliferation-promoting transcription factors JunB and c-Myc in myotubes and in muscle post-exercise.

Conclusions:

  • LIF is a contraction-induced myokine released by skeletal muscle.
  • LIF likely acts in an autocrine or paracrine manner to stimulate satellite cell proliferation.
  • LIF signaling contributes to exercise-induced muscle adaptation and repair through gene regulation.

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