Cochran D L, Wisner L A, Richards M F, Rouse C A
Department of Periodontics, Medical College of Virginia, Virginia Commonwealth University, Richmond 23284.
Arch Oral Biol. 1990;35(7):515-22. doi: 10.1016/0003-9969(90)90081-k.
Glycosaminoglycans specifically regulate the amount of calcium released from bone cultures; the mechanisms responsible for this regulation are not known. Media from glycosaminoglycan-stimulated bone organ cultures were analysed to determine (1) if specific calcium-releasing substances were selectively produced, and (2) if protein synthesis was differentially affected by glycosaminoglycans. Chondroitin sulphate B, hyaluronic acid and keratan sulphate at 100 micrograms/ml significantly increased prostaglandin release when compared with control cultures. In combination with suboptimal concentrations of PTH, chondroitin sulphate B, heparin and keratan sulphate significantly stimulated prostaglandin release. When indomethacin was included in the test assays, the stimulated prostaglandin release was abolished. Heparin-treated cultures released the greatest percentage of latent collagenase activity followed by hyaluronic acid-treated cultures. Organ cultures treated with heparin and PTH amount of active collagenase. Stimulation increased interleukin-1 above control levels but with no significant difference among the glycosaminoglycans except for keratan sulphate cultures with which had the greatest amount of interleukin-1. Collagen protein decreased between 48 and 72 h under both control and experimental conditions. Examination of the predominant [35S]-methionine labelled proteins revealed that prostaglandin E2 treatment resulted in a relative shift in labelling to higher molecular-weight proteins as time in culture increased (up to 144 h). After 48 h, when equal amounts of labelled protein were analysed, there was a predominance in labelling of a 200,000 Da protein in the prostaglandin-treated cultures. These findings demonstrate that modulation of calcium release by glycosaminoglycans results in the selective release of molecules capable of stimulating calcium release.(ABSTRACT TRUNCATED AT 250 WORDS)
糖胺聚糖特异性调节从骨培养物中释放的钙量；负责这种调节的机制尚不清楚。分析了来自糖胺聚糖刺激的骨器官培养物的培养基，以确定：（1）是否选择性产生了特定的钙释放物质；（2）蛋白质合成是否受到糖胺聚糖的不同影响。与对照培养物相比，100微克/毫升的硫酸软骨素B、透明质酸和硫酸角质素显著增加了前列腺素的释放。与次优浓度的甲状旁腺激素联合使用时，硫酸软骨素B、肝素和硫酸角质素显著刺激了前列腺素的释放。当在测试分析中加入吲哚美辛时，刺激的前列腺素释放被消除。肝素处理的培养物释放出最大比例的潜在胶原酶活性，其次是透明质酸处理的培养物。用肝素和甲状旁腺激素处理的器官培养物有活性胶原酶。刺激使白细胞介素-1高于对照水平，但除硫酸角质素培养物（其白细胞介素-1含量最高）外，糖胺聚糖之间无显著差异。在对照和实验条件下，胶原蛋白在48至72小时之间均减少。对主要的[35S]-甲硫氨酸标记蛋白的检查显示，随着培养时间的增加（长达144小时），前列腺素E2处理导致标记向更高分子量的蛋白相对转移。48小时后，当分析等量的标记蛋白时，前列腺素处理的培养物中200,000道尔顿蛋白的标记占优势。这些发现表明，糖胺聚糖对钙释放的调节导致了能够刺激钙释放的分子的选择性释放。（摘要截断于250字）
