Carbonic anhydrase II is induced in HL-60 cells by 1,25-dihydroxyvitamin D3: a model for osteoclast gene regulation.
Carbonic anhydrase II is induced in HL-60 cells by 1,25-dihydroxyvitamin D3: a model for osteoclast gene regulation.
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碳酸酐酶 II 在 HL-60 细胞中由 1,25-二羟基维生素 D3 诱导：破骨细胞基因调控模型。
DOI：
10.1016/0014-5793(89)80647-7
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发表时间：
1989
期刊：
影响因子：
3.5
通讯作者：
Tashian,RE
中科院分区：
文献类型：
--
作者：
HillstromShapiro,L;Venta,PJ;Yu,YS;Tashian,RE
碳酸酐酶II（CA II）产生破骨细胞介导的人体骨吸收所需的H+。我们已经开发了人早幼粒细胞系HL-60作为模型系统，研究破骨细胞特异性表达的CA II基因。用1，25-二羟维生素D3处理细胞系导致CA II在蛋白质和mRNA水平上的戏剧性从头诱导。CA II mRNA也诱导到较小程度的12-O-十四烷酰基佛波醇13-乙酸酯。二甲亚砜处理没有增加CA II mRNA。这些结果表明，HL-60细胞系将是一个有用的模型系统，研究破骨细胞特异性表达的CA II基因。
Carbonic anhydrase II (CA II) generates the H+required for osteoclast-mediated bone resorption in humans. We have developed the human promyelocytic cell line HL-60 as a model system with which to study the osteoclast-specific expression of the CA II gene. Treatment of the cell line with 1,25-dihydroxyvitamin D3resulted in a dramatic de novo induction of CA II at both the protein and mRNA levels. CA II mRNA was also induced to a lesser extent by 12-O-tetradecanoyl phorbol 13-acetate. Treatment with dimethyl sulfoxide did not increase CA II mRNA. These findings indicate that the HL-60 cell line will be a useful model system to study the osteoclast-specific expression of the CA II gene.