1,25-Dihydroxyvitamin D3 or dexamethasone modulate arachidonic acid uptake and distribution into glycerophospholipids by normal adult human osteoblast-like cells.
1,25-Dihydroxyvitamin D3 or dexamethasone modulate arachidonic acid uptake and distribution into glycerophospholipids by normal adult human osteoblast-like cells.
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1,25-二羟基维生素 D3 或地塞米松调节正常成人成骨细胞样细胞对花生四烯酸的摄取和分配到甘油磷脂中。
DOI：
10.1002/jcb.240570404
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Keeting,PE
中科院分区：
文献类型：
--
作者：
Cissel,DS;Birkle,DL;Whipkey,DL;Blaha,JD;Graeber,GM;Keeting,PE
研究了用促骨类固醇1，25-二羟基维生素D3（1，25（OH）2D3）、17 β-雌二醇或地塞米松处理对正常成人成骨细胞样（hOB）细胞摄取[1 - 14 C]花生四烯酸（AA）并分布到甘油磷脂类中的影响。当暴露于激素24、48或96小时后进行测定时，地塞米松处理的细胞中[1 - 14C] AA的总摄取减少。地塞米松处理48 h后，磷脂酰胆碱的特异性放射性标记掺入减少，同时磷脂酰乙醇胺的放射性标记增加。然而，这些变化是一过性的，地塞米松处理96 h后，放射性标记脂肪酸的分布重新平衡，与溶剂处理样品中发现的模式相似。1，25（OH）2D3处理96 h后，[1 - 14 C] AA的总摄取减少（对照的79 ± 3%，P <0.01）;在该时间点，磷脂酰肌醇池的放射性标记比例显著降低（对照的92 ± 2%，P <0.05）。发现[1 - 14 C] AA的总摄取和磷脂酰肌醇掺入的1，25（OH）2D3依赖性降低具有激素剂量依赖性。24，25（OH）2D3处理对总[1 - 14C] AA摄取或磷脂酰肌醇池的特异性[1 - 14C] AA放射性标记均无影响。1，25（OH）2D3处理降低了hOB细胞对[1 - 14C]油酸的摄取，并降低了其掺入磷脂酰肌醇池的比例。气相色谱分析显示，对总磷脂酰肌醇脂质质量或磷脂酰肌醇池中花生四烯酸的摩尔百分比无1，25（OH）2D3依赖性影响，因此开环甾类化合物对hOB细胞AA代谢的影响机制无法解释。17 β-雌二醇对测定的AA代谢参数无影响。由于它们调节花生四烯酸的摄取及其分布到hOB细胞磷脂中，类固醇可能会改变其他激素的生物效应，这些激素的作用包括刺激生物活性AA代谢物的产生，如野牡丹素或各种脂氧合酶产物。
The effects of treatment with the osteotropic steroids 1,25‐dihydroxyvitamin D3(1,25(OH)2D3), 17β‐estradiol, or dexamethasone on [1‐14C]arachidonic acid (AA) uptake and distribution into glycerophospholipid classes by normal adult human osteoblast‐like (hOB) cells were investigated. Total uptake of [1‐14C]AA was decreased in cells treated with dexamethasone when assayed after a 24‐, 48‐, or 96‐h exposure to the hormone. Specific radiolabel incorporation into phosphatidylcholine was reduced by a 48‐h treatment with dexamethasone with a concurrent increase in the radiolabeling of phosphatidylethanolamine. However, these changes were transient, and by 96 h of dexamethasone treatment the distribution of the radiolabeled fatty acid had reequilibrated to resemble the pattern found for vehicle treated samples. Total uptake of [1‐14C]AA was diminished by 96‐h treatment with 1,25(OH)2D3(79 ± 3% of control,P< 0.01); at that time point, a significant decrease in the proportional radiolabeling of the phosphatidylinositol pool was identified (92 ± 2% of control,P< 0.05). The 1,25(OH)2D3‐dependent decrease in total uptake and in phosphatidylinositol incorporation of [1‐14C]AA were found to be hormone dose dependent. Treatment with 24,25(OH)2D3was without effect on either total [1‐14C]AA uptake or the specific [1‐14C]AA radiolabeling of the phosphatidylinositol pool. 1,25(OH)2D3treatment decreased hOB cell uptake of [1‐14C]oleic acid and decreased its proportional incorporation into the phosphatidylinositol pool. Gas chromatographic analyses revealed no 1,25(OH)2D3‐dependent effects on total phosphatidylinositol lipid mass or on the mole percent of arachidonic acid within the phosphatidylinositol pool, leaving the mechanism of the effects of the secosteroid on hOB cell AA metabolism unexplained. 17β‐Estradiol had no effects on the parameters of AA metabolism measured. As a consequence of their modulation of arachidonic acid uptake and its distribution into hOB cellular phospholipids, steroids might alter the biological effects of other hormones whose actions include the stimulated production of bioactive AA metabolites, such as prostaglandins or the various lipoxygenase products.