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The neonatal sarcoplasmic reticulum Ca2+-ATPase gives a clue to development and pathology in human muscles

Magdolna Kósa1, Kitti Brinyiczki, Philip van Damme

  • 1Department of Biochemistry, Faculty of General Medicine, University of Szeged, Dóm tér 9, H-6720, Szeged, Hungary.

Journal of Muscle Research and Cell Motility
|December 10, 2014
PubMed

Insights

The sarcoplasmic/endoplasmic reticulum calcium ATPase 1 (SERCA1) has two isoforms, SERCA1a and SERCA1b. This study developed a method to assess their dominance in human muscles, revealing unique expression patterns and associations with muscular dystrophies.

Area of Science:

  • Molecular Biology
  • Muscle Physiology
  • Biochemistry

Background:

  • The sarcoplasmic/endoplasmic reticulum calcium ATPase 1 (SERCA1) gene exhibits two muscle-specific splice isoforms: SERCA1a (adult fast-type) and SERCA1b (neonatal/regenerating skeletal muscles).
  • The primary structural difference lies at the C-terminus: SERCA1a has a glycine, while SERCA1b possesses an octapeptide tail, complicating the development of isoform-specific antibodies.
  • The switch between SERCA1b and SERCA1a is a recognized marker of muscle differentiation.

Purpose of the Study:

  • To develop and validate a method for estimating the SERCA1b/SERCA1a ratio in human skeletal muscles using immunoblot analysis.
  • To investigate the expression patterns of SERCA1 isoforms in various human muscle tissues, including infant, neonatal, fetal, and adult samples.
  • To explore the association of SERCA1 isoform expression with specific muscle diseases, such as Duchenne muscular dystrophy and myotonic dystrophy type 2 (DM2).

Main Methods:

  • Development of a quantitative immunoblotting technique utilizing signal ratios from a SERCA1b-specific antibody and a pan-SERCA1 antibody.
  • Analysis of SERCA1 isoform dominance in human muscle biopsies from different age groups and developmental stages.
  • Comparative analysis of SERCA1 isoform expression in healthy individuals versus patients with Duchenne muscular dystrophy and DM2.

Main Results:

  • Unlike rodents, human SERCA1b expression was primarily observed in pre-matured infant leg and arm muscles, being replaced by SERCA1a in more mature neonatal muscles.
  • SERCA1b was undetectable in human fetal and neonatal diaphragms, with only SERCA1a detected in Duchenne muscular dystrophy patients (7-12 years old).
  • In adult DM2 patients, SERCA1b expression dominated over SERCA1a, indicating a distinct expression profile compared to rodents and specific disease associations.

Conclusions:

  • The human SERCA1b isoform exhibits a unique developmental and tissue-specific expression pattern distinct from that observed in rodents.
  • The SERCA1b/SERCA1a ratio serves as a valuable indicator of muscle differentiation and maturation in humans.
  • Aberrant SERCA1b expression is associated with specific neuromuscular conditions, notably myotonic dystrophy type 2 (DM2).

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