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Nicotinic acid adenine dinucleotide phosphate regulates skeletal muscle differentiation via action at two-pore

Parvinder K Aley1, Anna M Mikolajczyk, Barbara Munz

  • 1Department of Pharmacology, University of Oxford, Oxford OX1 3QT, United Kingdom.

Proceedings of the National Academy of Sciences of the United States of America
|November 3, 2010
PubMed

Insights

Nicotinic acid adenine dinucleotide phosphate (NAADP) signaling is vital for skeletal muscle differentiation. This study shows NAADP targets two-pore channels in acidic organelles to promote myoblast differentiation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Physiology

Background:

  • Calcium signaling is crucial for cell differentiation, particularly in skeletal muscle.
  • The precise mechanisms regulating skeletal muscle differentiation via calcium signaling are not fully understood.

Purpose of the Study:

  • To investigate the role of nicotinic acid adenine dinucleotide phosphate (NAADP) signaling in skeletal muscle differentiation.
  • To identify the specific calcium signaling pathways involved in myogenesis.

Main Methods:

  • Utilized skeletal muscle precursors and C2C12 cells.
  • Manipulated NAADP signaling pathways (interference and potentiation).
  • Employed siRNA knockdown of two-pore channels.

Main Results:

  • Interfering with NAADP signaling inhibited skeletal muscle differentiation.
  • Enhancing NAADP signaling potentiated differentiation.
  • Knockdown of two-pore channels attenuated differentiation, implicating them as NAADP targets.

Conclusions:

  • NAADP signaling plays a critical role in skeletal muscle differentiation.
  • NAADP acts on two-pore channels located in acidic organelles within myoblasts to drive differentiation.
  • The inositol trisphosphate pathway may play a minor role, while the ryanodine cascade is not involved.

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