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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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Vascular remodeling and arterial calcification are directly mediated by S100A12 (EN-RAGE) in chronic kidney disease

Joseph Gawdzik1, Liby Mathew, Gene Kim

  • 1Sections of Cardiology, Department of Medicine, University of Chicago, IL 60637, USA.

American Journal of Nephrology
|March 5, 2011
PubMed

Insights

The proinflammatory cytokine S100A12 (EN-RAGE) promotes vascular calcification in chronic kidney disease (CKD). This study shows S100A12 exacerbates CKD-induced vascular osteogenesis and calcification in mice via RAGE activation and oxidative stress.

Area of Science:

  • Cardiovascular Biology
  • Nephrology
  • Vascular Biology

Background:

  • The proinflammatory cytokine S100A12 (EN-RAGE) is linked to cardiovascular issues in hemodialysis patients.
  • This study investigates S100A12's role in vascular disease development under chronic kidney disease (CKD) conditions.

Purpose of the Study:

  • To test if S100A12 expression in vascular smooth muscle contributes to vascular disease in a CKD mouse model.
  • To elucidate the mechanisms by which S100A12 influences vascular calcification in CKD.

Main Methods:

  • Chronic kidney disease (CKD) was induced in S100A12 transgenic and wild-type mice via ureter ligation.
  • Aortic tissues and cultured aortic smooth muscle cells were analyzed after 7 weeks of elevated blood urea nitrogen (BUN).

Main Results:

  • S100A12 transgenic mice exhibited enhanced vascular medial calcification compared to wild-type mice with CKD.
  • Vascular calcification involved the S100A12 receptor, RAGE (receptor for advanced glycation endproducts), and oxidative stress.
  • Inhibiting NADPH-oxidase Nox1 or RAGE signaling attenuated calcification and osteoblastic gene expression in cultured cells.

Conclusions:

  • S100A12 significantly augments CKD-triggered vascular osteogenesis in mice.
  • These findings mirror vascular calcification observed in human CKD and end-stage kidney disease patients.
Abstract

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