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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
08:43

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

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Endogenous bone morphogenetic protein 2 plays a role in vascular smooth muscle cell calcification induced by

Mingshu Sun1, Qing Chang2, Miaomiao Xin1

  • 11 Department of Rheumatology and Clinical Immunology, the Affiliated Hospital of Qingdao University, Qingdao, China.

International Journal of Immunopathology and Pharmacology
|January 31, 2017
PubMed

Insights

Interleukin-6 (IL-6) promotes vascular calcification in rheumatoid arthritis by inducing osteogenic differentiation in smooth muscle cells via bone morphogenetic protein-2 (BMP2). This highlights a key mechanism in RA cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Rheumatology
  • Cellular and Molecular Medicine

Background:

  • Systemic inflammation, particularly elevated serum interleukin-6 (IL-6), is linked to vascular calcification and cardiovascular disease, the primary cause of mortality in rheumatoid arthritis (RA).
  • The precise mechanisms by which IL-6 contributes to vascular calcification in RA remain incompletely understood.

Purpose of the Study:

  • To investigate the role of IL-6 in vascular calcification using a human umbilical artery smooth muscle cell (HUASMC) culture model.
  • To elucidate the molecular pathways, specifically the involvement of bone morphogenetic protein-2 (BMP2), through which IL-6 induces calcification.

Main Methods:

  • Cultured HUASMCs were treated with recombinant human IL-6 (rhIL-6) to assess calcification.
  • Measured calcium deposition, calcium concentration, and mRNA/protein levels of BMP2, bone-specific alkaline phosphatase (BAP), osteoprotegerin (OPG), and osteopontin (OPN).
  • Utilized anti-BMP2 small interfering RNA (siRNA) to investigate BMP2's role in rhIL-6-induced calcification.

Main Results:

  • rhIL-6 significantly induced calcification and osteogenic differentiation in HUASMCs in a time- and dose-dependent manner.
  • rhIL-6 upregulated the expression of BMP2, BAP, OPG, and OPN.
  • Knockdown of BMP2 using siRNA partially inhibited rhIL-6-induced calcification and reduced the expression of associated osteogenic markers.

Conclusions:

  • Recombinant human IL-6 induces extracellular calcification and osteogenic differentiation of human artery smooth muscle cells in vitro.
  • This effect is mediated, at least in part, through the upregulation of endogenous BMP2.
  • The IL-6/BMP2 pathway represents a potential mechanism underlying vascular calcification in rheumatoid arthritis.

Keywords:
RNA interferingbone morphogenetic protein 2interleukin 6rheumatoid arthritisvascular calcification

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