Exposure of aortic vascular smooth muscle cells to low-frequency electromagnetic field inhibits osteopontin expression and matrix metalloproteinase activity.
Primary cultured rat aortic vascular smooth muscle cells (VSMCs) were exposed to different intensities of low-frequency electromagnetic fields (LFEMFs) at 20, 40, and 60 mT for different time periods (10, 20, and 30 minutes). Furthermore, osteopontin (OPN) mRNA and protein expressions were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively. Matrix metalloproteinase-2 (MMP-2) activity was measured using gelatin zymography. The results showed that the OPN mRNA and protein expressions and MMP-2 activity of VSMCs were inhibited by exposure to LFEMFs of different intensities in a dose-dependent manner (P < 0.05) but not in a time-dependent manner. In conclusion, exposure to LFEMFs of appropriate intensity for a suitable time period can result in the inhibition of the OPN expression and MMP-2 activity of VSMCs, indicating the potential prophylactic and therapeutic effects of LFEMFs on restenosis (RS) following percutaneous coronary intervention (PCI).
Hu
Tao
T
Beijing University of Technology, Beijing, China.
Li
Huan
H
Zhang
Xiaojun
X
Luan
Ronghua
R
Li
Chengxiang
C
Cheng
Hexiang
H
Wang
Haichang
H
Li
Xiaoyang
X
Zeng
Yanjun
Y
D000818:Animals; D001011:Aorta / Q000166:cytology / Q000378:metabolism / Q000528:radiation effects; D018929:Cell Culture Techniques; D004574:Electromagnetic Fields; D006083:Graft Occlusion, Vascular / Q000628:therapy; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism* / Q000528:radiation effects*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism* / Q000528:radiation effects*; D053495:Osteopontin / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
D012333:RNA, Messenger; D053495:Osteopontin; D020778:Matrix Metalloproteinase 2