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Effects of electromagnetic stimuli on bone and bone cells in vitro: Inhibition of responses to parathyroid hormone by low-energy low-frequency fields

机译:电磁刺激对骨骼和骨细胞的体外影响:低能量低频场抑制对甲状旁腺激素的反应

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摘要

Low-energy electromagnetic fields pulsed at frequencies of 10-90 Hz significantly increase healing of chronic fracture nonunions in man. These fields are effective at tissue current levels several orders of magnitude lower than those required for transmembrane depolarization of normal cells. We have examined the effects of two clinically used pulsed electromagnetic fields on cultures of the osteoblast-like mouse bone cell line MMB-1. Both fields significantly reduced cellular production of cAMP in response to parathyroid hormone and osteoclast activating factor. Neither basal nor fluoride-activated levels of adenylate cyclase were altered in membranes from cells cultured in the fields; however, the same membrane preparations exhibited markedly inhibited responses to parathyroid hormone. The fields blocked the inhibitory effects of the hormone on collagen synthesis by MMB-1 cells. However, there was no effect on the inhibition of collagen synthesis by 1,25-dihydroxyvitamin D3, which is believed to act primarily by a nuclear, rather than by a membrane-dependent, mechanism. No significant differences were noted between effects of the two fields, one generating continuous pulse trains (72 Hz) and the other generating recurrent bursts (15 Hz) of shorter pulses. We hypothesize that these field effects are mediated primarily at the plasma membrane of osteoblasts, either by interference with hormone-receptor interactions or by blocking of receptor-cyclase coupling in the membrane. These responses occurred with induced extracellular fields of 1 mV/cm or less, even though transmembrane potential gradients are typically 105 V/cm.
机译:以10-90 Hz的频率脉冲的低能电磁场显着提高了人类慢性骨折骨不连的愈合。这些场在比正常细胞跨膜去极化所需的组织电流水平低几个数量级的情况下有效。我们已经检查了两种临床上使用的脉冲电磁场​​对成骨样小鼠骨细胞系MMB-1的培养的影响。响应甲状旁腺激素和破骨细胞活化因子,这两个领域都显着降低了cAMP的细胞产生。在田间培养的细胞膜中,腺苷酸环化酶的基础水平或氟化物激活水平均未改变;然而,相同的膜制剂对甲状旁腺激素的反应明显受到抑制。该领域阻断了该激素对MMB-1细胞胶原合成的抑制作用。但是,1,25-二羟基维生素D3对胶原蛋白合成的抑制作用没有影响,据信这主要是通过核机制而不是膜依赖性机制起作用。在这两个场的影响之间没有观察到显着差异,一个场产生连续的脉冲序列(72 Hz),另一个场产生较短脉冲的循环突发(15 Hz)。我们假设这些场效应主要是通过干扰激素-受体相互作用或通过阻断膜中受体-环化酶偶联而在成骨细胞质膜上介导的。即使跨膜电位梯度通常为105 V / cm,在诱导的1 mV / cm或更小的细胞外电场下也会发生这些反应。

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