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Magnesium and cell proliferation.

M E Maguire1

  • 1Department of Pharmacology, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106.

Annals of the New York Academy of Sciences
|January 1, 1988
PubMed
Summary

Magnesium (Mg2+) deficiency impairs cell growth and hormone response by altering receptor-G-protein coupling. This study develops methods to investigate Mg2+ regulation in cells, revealing specific impacts on cellular processes.

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Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry·1999

Area of Science:

  • Cell Biology
  • Biochemistry
  • Physiology

Background:

  • Magnesium (Mg2+) is crucial for cell growth and hormone response, but its intracellular regulation is not fully understood.
  • Developing methods to dynamically measure intracellular free Mg2+ is essential for studying its roles.
  • Mg2+-deficient cell models are needed to investigate the consequences of low Mg2+ levels.

Purpose of the Study:

  • To develop and utilize methods for studying Mg2+ regulation of cell growth and hormonal response.
  • To characterize Mg2+-deficient cell lines and their physiological responses.
  • To elucidate the specific effects of Mg2+ deficiency on receptor-mediated signaling pathways.

Main Methods:

  • Development of cell-permeable Mg2+ indicators for dynamic intracellular concentration measurement.
  • Establishment and characterization of "Mg2+-deficient" murine S49 lymphoma cell lines.
  • Analysis of hormonal responses, receptor-G-protein coupling, and Mg2+ transport in deficient cells.
  • Validation of S49 cell model using T-lymphocytes from Mg2+-deficient rats.

Main Results:

  • Mg2+-deficient S49 cells exhibit slower growth rates (doubling times of 22 and 60 hours) compared to wild-type cells (17 hours).
  • Total cell Mg2+ decreased by 50%, with a selective 75% reduction in cytoplasmic Mg2+ while particulate Mg2+ remained unchanged.
  • Hormonal response was significantly impaired; cyclic AMP accumulation upon beta-adrenergic receptor activation decreased by over 95%.
  • Response to PGE1 receptor activation was reduced by only 50%, indicating differential effects on signaling pathways.
  • Mg2+ transport remained at wild-type rates but showed higher affinity and lost hormone sensitivity.
  • Ca2+ content was normal or slightly elevated in Mg2+-deficient cells.
  • Similar results were observed in T-lymphocytes from Mg2+-deficient rats, validating the S49 cell model.

Conclusions:

  • Mg2+ deficiency leads to significant growth abnormalities in mammalian cells.
  • Reduced Mg2+ markedly alters receptor-G-protein coupling, impacting cellular signaling pathways.
  • The effects of Mg2+ deficiency appear more pronounced on receptor-G-protein interactions than on G-protein-adenylate cyclase activity.
  • The developed Mg2+-deficient S49 lymphoma cell lines serve as a valuable model for studying Mg2+ homeostasis and its physiological consequences.

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