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Receptor for advanced glycation end products involved in circulating endothelial cells release from human coronary

Shulai Zhou1, Lichao Gao1, Fangqi Gong1

  • 1Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310003 China.

Iranian Journal of Basic Medical Sciences
|July 30, 2015
PubMed

Insights

C-reactive protein (CRP) increases circulating endothelial cells (CECs) release from coronary artery cells, mediated by the receptor for advanced glycation end products (RAGE). Silencing RAGE reduces this effect, suggesting RAGE as a therapeutic target for cardiovascular diseases.

Area of Science:

  • Cardiovascular Biology
  • Endothelial Cell Biology
  • Molecular Medicine

Background:

  • Endothelial dysfunction is a key factor in cardiovascular diseases.
  • Circulating endothelial cells (CECs) are markers of endothelial injury.
  • The role of receptor for advanced glycation end products (RAGE) in CEC release is not fully understood.

Purpose of the Study:

  • To investigate the impact of C-reactive protein (CRP) and S100A12 on CEC release from human coronary artery endothelial cells (HCAECs).
  • To determine the involvement of RAGE in CRP-induced CEC release.

Main Methods:

  • HCAECs were treated with varying concentrations of CRP or S100A12.
  • CEC release was quantified using flow cytometry.
  • RAGE expression was reduced using small interfering RNA (siRNA) to assess its role.

Main Results:

  • CRP significantly increased CEC release from HCAECs in a dose-dependent manner.
  • S100A12 did not affect CEC release.
  • Silencing RAGE with siRNA attenuated the CRP-induced increase in CEC release.

Conclusions:

  • RAGE plays a critical role in CRP-mediated CEC release.
  • Inhibition of RAGE may offer a therapeutic strategy for endothelial dysfunction in cardiovascular diseases.
  • Targeting RAGE could be beneficial for treating coronary artery lesions, particularly in Kawasaki disease.
Abstract

Keywords:
CECsCRPHCAECsRAGES100A12

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