title: Enhanced responsiveness to parathyroid hormone and induction of functional differentiation of cultured rabbit costal chondrocytes by a pulsed electromagnetic field.
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.
authors.affiliation: Department of Biochemistry and Calcified-Tissue Metabolism, Faculty of Dentistry, Osaka University, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Hiraki
authors.forename: N
authors.initials: N
authors.lastname: Endo
authors.forename: M
authors.initials: M
authors.lastname: Takigawa
authors.forename: A
authors.initials: A
authors.lastname: Asada
authors.forename: H
authors.initials: H
authors.lastname: Takahashi
authors.forename: F
authors.initials: F
authors.lastname: Suzuki
mesh_terms: D000527:Alprostadil / Q000494:pharmacology; D000818:Animals; D002356:Cartilage / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D002454:Cell Differentiation; D002478:Cells, Cultured; D000242:Cyclic AMP / Q000378:metabolism; D004574:Electromagnetic Fields; D055590:Electromagnetic Phenomena; D004790:Enzyme Induction / Q000187:drug effects; D011464:Epoprostenol / Q000494:pharmacology; D006025:Glycosaminoglycans / Q000096:biosynthesis; D008297:Male; D009955:Ornithine Decarboxylase / Q000096:biosynthesis; D010281:Parathyroid Hormone / Q000494:pharmacology*; D011817:Rabbits; D013431:Sulfates / Q000378:metabolism
chemical_list: D006025:Glycosaminoglycans; D010281:Parathyroid Hormone; D013431:Sulfates; D011464:Epoprostenol; D000242:Cyclic AMP; D009955:Ornithine Decarboxylase; D000527:Alprostadil