[Effect of inflammatory factors on cell proliferation and apoptosis in insulin-like grown factor 1-slienced human coronary artery smooth muscle cells]

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2014 Apr;36(2):176-9. doi: 10.3881/j.issn.1000-503X.2014.02.011.
[Article in Chinese]

Abstract

Objective: To study the effect of inflammatory factors on cell proliferation and apoptosis in insulin-like grown factor 1 (IGF1)-slienced human coronary artery smooth muscle cells (hCASMCs).

Methods: We silenced the expression of IGF1 in hCASMCs using the lentivirus-mediated RNA interference technology. Blank control group and negative control group were set using the hCASMCs without the infection of a virus vector and the hCASMCs with the infection of a negative control virus vector, respectively. After the treatment of these cells with both tumor necrosis factor-α 50 ng/ml and interleukin-1β 40 ng/ml, the concentration of IGF1 in cell-culture medium was detected by enzyme-linked immunosorbent assay, and the proliferation and apoptosis were evaluated by MTT assay and flow cytometry.

Results: After the simulation with inflammatory factors, the concentration of IGF1 in the supernatant fluid of cultured IGF1-slienced hCASMCs was significantly lower than those in the blank control group and negative control group [(426.35±120.96) vs. (1 030.69±54.69) and (992.82±26.90)pg/ml, P=0.000). The proliferation of IGF1-slienced hCASMCs was substantially much less than the two control groups (0.302±0.011 vs. 0.401±0.028 and 0.302±0.011, F=37.628, P=0.000), and the apoptosis rate of IGF1-slienced hCASMCs was significant increased compared with the other two groups [(10.57±0.99)% vs. (0.19±0.13)% and (1.31±0.30)%, P=0.001].

Conclusion: Inflammatory factors can inhibit the cell proliferation and promote apoptosis after the knock-down of IGF1 in hCASMCs.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis*
  • Cell Proliferation / drug effects
  • Coronary Vessels / cytology*
  • Humans
  • Insulin-Like Growth Factor I / genetics
  • Insulin-Like Growth Factor I / metabolism*
  • Interleukin-1beta / pharmacology*
  • Myocytes, Smooth Muscle / drug effects*
  • RNA Interference
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • IGF1 protein, human
  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha
  • Insulin-Like Growth Factor I