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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

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17beta-estradiol signaling in skeletal muscle cells and its relationship to apoptosis

Ricardo Boland1, Andrea Vasconsuelo, Lorena Milanesi

  • 1Departamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, San Juan 670, 8000 Bahia Blanca, Argentina. rboland@criba.edu.ar

Steroids
|February 15, 2008
PubMed

Insights

17beta-estradiol protects skeletal muscle cells from apoptosis via non-genomic pathways involving ERalpha and ERbeta. This mechanism activates ERK1/2 and PI3K/Akt, crucial for preventing cell death in muscle tissue.

Area of Science:

  • Cell Biology
  • Endocrinology
  • Muscle Physiology

Background:

  • Estrogen signaling plays a critical role in cellular function.
  • Skeletal muscle health is influenced by hormonal balance.
  • Apoptosis, or programmed cell death, is a key factor in muscle degeneration.

Purpose of the Study:

  • To investigate the antiapoptotic mechanisms of 17beta-estradiol in skeletal muscle cells.
  • To elucidate the roles of estrogen receptor alpha (ERalpha) and estrogen receptor beta (ERbeta) in this process.
  • To explore the involvement of non-genomic signaling pathways.

Main Methods:

  • Primary skeletal muscle cell cultures.
  • Western blotting to assess protein activation (ERK1/2, PI3K/Akt, BAD phosphorylation).
  • Mitochondrial function assays.
  • Apoptosis assays.

Main Results:

  • 17beta-estradiol demonstrated a significant antiapoptotic effect in skeletal muscle cells.
  • This protection was mediated by extranuclear ERalpha and ERbeta.
  • Key non-genomic pathways activated include ERK1/2 and PI3K/Akt, leading to BAD phosphorylation.
  • ERbeta was particularly important for inhibiting apoptosis at the mitochondrial level.
  • Both ERalpha and ERbeta contributed equally to Akt activation.

Conclusions:

  • 17beta-estradiol confers antiapoptotic protection to skeletal muscle cells through extranuclear estrogen receptors.
  • Non-genomic signaling via ERK1/2 and PI3K/Akt pathways is central to this protective effect.
  • Differential roles of ERalpha and ERbeta in apoptosis regulation suggest isoform-specific functions within the cell.
  • Estrogen deficiency-related myopathies may stem from impaired estrogen-mediated apoptosis regulation.

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