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脉冲电磁场增强培养的兔肋软骨细胞对甲状旁腺激素的反应性并诱导其功能分化。

Enhanced responsiveness to parathyroid hormone and induction of functional differentiation of cultured rabbit costal chondrocytes by a pulsed electromagnetic field.

作者信息

Hiraki Y, Endo N, Takigawa M, Asada A, Takahashi H, Suzuki F

机构信息

Department of Biochemistry and Calcified-Tissue Metabolism, Faculty of Dentistry, Osaka University, Japan.

出版信息

Biochim Biophys Acta. 1987 Oct 22;931(1):94-100. doi: 10.1016/0167-4889(87)90054-1.

DOI:10.1016/0167-4889(87)90054-1
PMID:2820512
Abstract

Pulsed electromagnetic fields promote healing of delayed united and ununited fractures by triggering a series of events in fibrocartilage. We examined the effects of a pulsed electromagnetic field (recurrent bursts, 15.4 Hz, of shorter pulses of an average of 2 gauss) on rabbit costal chondrocytes in culture. A pulsed electromagnetic field slightly reduced the intracellular cyclic adenosine 3',5'-monophosphate (cAMP) level in the culture. However, it significantly enhanced cAMP accumulation in response to parathyroid hormone (PTH) to 140% of that induced by PTH in its absence, while it did not affect cAMP accumulation in response to prostaglandin E1 or prostaglandin I2. The effect on cAMP accumulation in response to PTH became evident after exposure of the cultures to the pulsed electromagnetic field for 48 h, and was dependent upon the field strength. cAMP accumulation in response to PTH is followed by induction of ornithine decarboxylase, a good marker of differentiated chondrocytes, after PTH treatment for 4 h. Consistent with the enhanced cAMP accumulation, ornithine decarboxylase activity induced by PTH was also increased by the pulsed electromagnetic field to 170% of that in cells not exposed to a pulsed electromagnetic field. Furthermore, stimulation of glycosaminoglycan synthesis, a differentiated phenotype, in response to PTH was significantly enhanced by a pulsed electromagnetic field. Thus, a pulsed electromagnetic field enhanced a series of events in rabbit costal chondrocytes in response to PTH. These findings show that exposure of chondrocytes to a pulsed electromagnetic field resulted in functional differentiation of the cells.

摘要

脉冲电磁场通过引发纤维软骨中的一系列事件来促进延迟愈合和不愈合骨折的愈合。我们研究了脉冲电磁场(重复脉冲,15.4赫兹,平均2高斯的较短脉冲)对培养的兔肋软骨细胞的影响。脉冲电磁场略微降低了培养物中细胞内的环磷酸腺苷(cAMP)水平。然而,它显著增强了软骨细胞对甲状旁腺激素(PTH)的反应,使cAMP积累量增加到在无脉冲电磁场时PTH诱导量的140%,而对前列腺素E1或前列腺素I2刺激引起的cAMP积累没有影响。在将培养物暴露于脉冲电磁场48小时后,对PTH引起的cAMP积累的影响变得明显,并且这取决于场强。在PTH处理4小时后,对PTH的反应中cAMP积累之后会诱导鸟氨酸脱羧酶,这是分化软骨细胞的一个良好标志物。与增强的cAMP积累一致,PTH诱导的鸟氨酸脱羧酶活性也因脉冲电磁场而增加到未暴露于脉冲电磁场的细胞中的170%。此外,脉冲电磁场显著增强了对PTH反应的糖胺聚糖合成(一种分化表型)。因此,脉冲电磁场增强了兔肋软骨细胞对PTH的一系列反应。这些发现表明,软骨细胞暴露于脉冲电磁场会导致细胞的功能分化。

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Enhanced responsiveness to parathyroid hormone and induction of functional differentiation of cultured rabbit costal chondrocytes by a pulsed electromagnetic field.脉冲电磁场增强培养的兔肋软骨细胞对甲状旁腺激素的反应性并诱导其功能分化。
Biochim Biophys Acta. 1987 Oct 22;931(1):94-100. doi: 10.1016/0167-4889(87)90054-1.
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Polyamine and differentiation: induction of ornithine decarboxylase by parathyroid hormone is a good marker of differentiated chondrocytes.多胺与分化:甲状旁腺激素诱导鸟氨酸脱羧酶是分化软骨细胞的良好标志物。
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Induction by parathyroid hormone of ornithine decarboxylase in rabbit costal chondrocytes in culture.甲状旁腺激素对培养的兔肋软骨细胞中鸟氨酸脱羧酶的诱导作用。
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The effect of parathyroid hormone (1-34) on cyclic AMP level, ornithine decarboxylase activity, and glycosaminoglycan synthesis of chondrocytes from mandibular condylar cartilage, nasal septal cartilage, and spheno-occipital synchondrosis in culture.甲状旁腺激素(1-34)对培养的下颌髁突软骨、鼻中隔软骨和蝶枕软骨结合处软骨细胞中环磷酸腺苷水平、鸟氨酸脱羧酶活性及糖胺聚糖合成的影响。
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Effects of various tumor promoters on expression of cartilage phenotypes in rabbit costal chondrocytes in culture.多种肿瘤启动子对培养的兔肋软骨细胞软骨表型表达的影响。
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