Sömjen D, Kaye A M, Binderman I
Biochem J. 1985 Feb 1;225(3):591-6. doi: 10.1042/bj2250591.
Bone cells in culture responded to parathyroid hormone (PTH) and prostaglandin E2 (PGE2) by a 2-fold increase in creatine kinase (CK) activity. Combined treatment resulted in a higher response than with PTH alone. Calcitonin (CT) failed to stimulate CK activity, did not affect the response of CK to PTH, but inhibited slightly the increase in CK activity by PGE2. Bone-cell cultures grown in low [Ca2+] (0.125 mM), enriched in PTH-responsive osteoblast-like cells, responded to PTH, but not to PGE2 or CT, by increased CK activity. In both normal and low-[Ca2+] cultures, 8-bromo cyclic AMP did not affect CK activity, nor did it change the response of the cells to PTH, PGE2 or CT. The increase in CK activity was time- and dose-dependent and inhibited both by cycloheximide and by actinomycin D. The isoenzyme of CK stimulated was the CKBB form, the isoenzyme induced by other hormones. This appears to be the first report of the stimulation of CK activity by a polypeptide hormone or a prostaglandin. We suggest that stimulation of CKBB can serve as a marker for the action of a variety of hormones and growth promoters.
培养中的骨细胞对甲状旁腺激素(PTH)和前列腺素E2(PGE2)产生反应,肌酸激酶(CK)活性增加了两倍。联合治疗比单独使用PTH产生更高的反应。降钙素(CT)未能刺激CK活性,不影响CK对PTH的反应,但略微抑制PGE2引起的CK活性增加。在低[Ca2+](0.125 mM)中生长的骨细胞培养物富含对PTH反应性的成骨细胞样细胞,通过增加CK活性对PTH产生反应,但对PGE2或CT无反应。在正常和低[Ca2+]培养物中,8-溴环磷酸腺苷均不影响CK活性,也不改变细胞对PTH、PGE2或CT的反应。CK活性的增加具有时间和剂量依赖性,并且受到环己酰亚胺和放线菌素D的抑制。被刺激的CK同工酶是CKBB形式,即由其他激素诱导的同工酶。这似乎是关于多肽激素或前列腺素刺激CK活性的首次报道。我们认为,CKBB的刺激可作为多种激素和生长促进剂作用的标志物。