Low strength static magnetic field inhibits the proliferation, migration, and adhesion of human vascular smooth muscle cells in a restenosis model through mediating integrins β1-FAK, Ca2+ signaling pathway.
The proliferation, migration, and adhesion of vascular smooth muscle cells (VSMCs) and their interactions with extracellular matrix are key features of atherosclerosis and restenosis. Recently, there has been evidence that magnetic fields exert multiple effects on the biological performance of cells and may aid in the treatment of vascular disease. However, the effect of a static magnetic field (SMF) on human VSMCs still remains unknown. In this study, we aimed to determine the effects of low strength SMF on human VSMCs in an in vitro restenosis model. A SMF was established using neodymium-yttrium-iron permanent magnet. Human umbilical artery smooth muscle cells (hUASMCs) were isolated and seeded to a fibronectin-coated plate to form an in vitro restenosis model and then exposed to a vertically oriented field of 5 militesla (mT). MTT, transwell, and adhesion assays were used to demonstrate that the proliferation, migration, and adhesion potential of hUASMCs were significantly decreased after exposure to 5 mT SMF for 48 h compared with a non-treated group. Meanwhile, confocal microscopy analysis was used to demonstrate that integrin β(1) clustering was inhibited by exposure to 5 mT SMF. Furthermore, the phosphorylation of focal adhesion kinase (FAK) was markedly inhibited, and the upregulated cytosolic free calcium had been reversed (p < 0.05). However, the biological effects of low strength SMF on hUASMCs could be blocked by the administration of GRGDSP-the blockade of integrins. In conclusion, a low strength SMF can influence the proliferation, migration, and adhesion of VSMCs by inhibiting the clustering of integrin β1, decreasing cytosolic free calcium concentration, and inactivating FAK. With further validation, SMFs may aid in attenuating abnormal VSMCs biological performance and has potential to block atherogenesis and prevent restenosis.
Department of Cardiovascular Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, People's Republic of China. fireman@fmmu.edu.cn
Yan
Y
Li
Li-Qiang
LQ
Song
Michael Q
MQ
Chen
Ying-Mei
YM
Zhang
Jingxia
J
Li
Xu-Yang
XY
Feng
Weijie
W
Li
Wenyi
W
Guo
Guoliang
G
Jia
Haichang
H
Wang
Jin
J
Yu
D002448:Cell Adhesion / Q000187:drug effects; D002465:Cell Movement; D049109:Cell Proliferation; D051417:Focal Adhesion Kinase 1 / Q000378:metabolism; D006083:Graft Occlusion, Vascular / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D016023:Integrins / Q000378:metabolism*; D060526:Magnetic Fields; D008954:Models, Biological; D009131:Muscle, Smooth, Vascular / Q000378:metabolism* / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000378:metabolism* / Q000473:pathology; D009842:Oligopeptides / Q000494:pharmacology; D010766:Phosphorylation / Q000187:drug effects; D014469:Umbilical Arteries / Q000378:metabolism / Q000473:pathology
D016023:Integrins; D009842:Oligopeptides; C058161:glycyl-arginyl-glycyl-aspartyl-seryl-proline; D051417:Focal Adhesion Kinase 1; C496050:PTK2 protein, human