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Etidronate prevents dystrophic cardiac calcification by inhibiting macrophage aggregation

Carolin Bauer1, Olivier le Saux2, Viola Pomozi2

  • 1Institute for Cardiogenetics, Universität zu Lübeck; DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Germany, University Heart Centre Lübeck, 23562, Lübeck, Germany.

Scientific Reports
|April 13, 2018
PubMed

Insights

Macrophages and multinucleated cells drive cardiovascular calcification. Inorganic pyrophosphate (PPi) and Etidronate show potential as inhibitors, while ICAM-1 plays a key role in this vascular disease process.

Area of Science:

  • Vascular Biology
  • Immunology
  • Biochemistry

Background:

  • Cardiovascular calcification is a significant risk factor for vascular disease.
  • Macrophage infiltration and osteoclast-related processes are implicated in calcification.
  • Genetic factors influence susceptibility to calcification, as seen in C3H vs. B6 mice.

Purpose of the Study:

  • To investigate the role of macrophages and multinucleated (MN) cells in cardiovascular calcification.
  • To explore the potential of inorganic pyrophosphate (PPi) and Etidronate as calcification inhibitors.
  • To identify key molecular players, such as ICAM-1, in the calcification process.

Main Methods:

  • Isolation and in vitro differentiation of splenic monocytes into macrophages using M-CSF.
  • Induction of multinucleated (MN) cell formation with RANKL.
  • Analysis of conditioned media from macrophages for calcification-inducing/inhibiting properties.
  • Measurement of ICAM-1 levels and plasma inorganic pyrophosphate (PPi) in mouse models.
  • In vivo administration of PPi or Etidronate to C3H mice.

Main Results:

  • Monocytes from calcification-resistant (B6) mice formed significantly fewer MN cells compared to susceptible (C3H) mice.
  • Conditioned media from C3H macrophages promoted calcification, while B6 macrophage media inhibited it.
  • Elevated ICAM-1 levels were observed in C3H macrophage media; PPi levels were lower in C3H mice.
  • PPi or Etidronate supplementation prevented cardiac calcification in C3H mice, but did not fully reverse it.

Conclusions:

  • Macrophages and MN cells are key players in the pathogenesis of tissue calcification.
  • Inorganic pyrophosphate (PPi) or its analogue Etidronate may serve as potential inhibitors of MN formation and calcification.
  • The adhesion molecule ICAM-1 plays a crucial role in cardiovascular calcification processes.

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