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ASSA13-03-31 In Vitro Investigations on the Effects of Arsenic Trioxide on Human Coronary Artery Smooth Muscle Cells, Endothelial Cells and EMAP-II
  1. Luan Tianzhu1,
  2. Xu Qinglu1,
  3. Fu Songbin2,
  4. Li Weimin1,
  5. Huang Yonglin1,
  6. Ji Hongliang3,
  7. Zhou Lijun1
  1. 1Department of Cardiology, The First Affiliated Hospital of Harbin Medical University
  2. 2Department of Biology, Harbin Medical University
  3. 3Department of Surgery, The First Affiliated Hospital of Harbin Medical University

Abstract

Objective To investigate the effects of arsenic trioxide on human coronary artery smooth muscle cells, endothelial cells and expres-sion of EMAP-II in the extracellular matrix.

Methods Human coronary artery smooth muscle cell line (HCASMC) and Coronary artery endothelial cell line (HCAEC) were incubated with different concentration of As2O3. Apoptosis of HCASMC and HCAEC were detected by situ apoptosis detection kit (TUNEL) and Flow cytometry respectively, Bax, Bcl-2 and EMAP-II expression were determined by Western blot, HCASMC mRNA was examined by applying Real-time PCR.

Results With the increase in the concentration of arsenic trioxide, it can inhibit the proliferation of HCSMC and the inhibitory effects were positively related to the duration and the concentration of arsenic trioxide (the viable count at the seventh day during the observation was (4.41 ± 0.10) × 105/ml when the concentration of it was 5.0 µmol/L, while the viable count in the normal control group was (30.11 ± 0.93) × 105/ml. The difference was statistically significant, P < 0.05). The apoptosis rate of HCEC significantly increased after 4.0 and 5.0 µmol/L arsenic trioxide was applied for 48 hours (P < 0.05), while 3.0 µmol/L and lower concentrations of arsenic trioxide had no significant apoptosis-promoting effects on endothelial cells. Arsenic trioxide up-regulated the expression of Bax gene but down-regulated the expression of the apoptosis inhibiting gene Bcl-2. Expression of E2F-1mRNA was the lowest at 48 h (P < 0.05). Expression of EMAP-II in the 48h group was the lowest and the cell adhesion rate was the lowest (P < 0.05). The above-mentioned typical changes were not observed in the normal control group.

Conclusions Arsenic trioxide could promote the apoptosis of HCSMC, reduce the expression of HCASMC transcription factor E2F-1 mRNA and EMAP-II in the extracellular matrix, and a certain concentration of arsenic trioxide had no significant effects on the re-endothelialization of blood vessels.

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