Kohno M, Takahashi S, Oida K, Suzuki J, Tamai T, Yamamoto T, Nakai T
Third Department of Internal Medicine, Fukui Medical School, Japan.
Atherosclerosis. 1997 Aug;133(1):45-9. doi: 10.1016/s0021-9150(97)00112-3.
Expression of VLDL receptor mRNA during differentiation of HL-60 cells was investigated by Northern analysis. The expression induced in 1 alpha,25-dihydroxyvitamin D3 (1 alpha,25(OH)2D3)-treated cells was 3 times that in untreated cells, while LDL receptor mRNA expression was unchanged. VLDL receptor mRNA levels were not changed in macrophages caused to differentiate from HL-60 cells by treatment with phorbol 12-myristate 13-acetate (PMA). Treatment of sarcoma cells which possess the vitamin D receptor (MG-63 cell line) with 1 alpha,25(OH)2D3 did not affect VLDL receptor mRNA levels. Therefore, 1 alpha,25(OH)2D3 induces VLDL receptor mRNA in HL-60 cells through differentiation-dependent mechanisms.
通过Northern分析研究了HL-60细胞分化过程中极低密度脂蛋白受体（VLDL受体）mRNA的表达。1α,25-二羟基维生素D3（1α,25(OH)2D3）处理的细胞中诱导的表达是未处理细胞中的3倍，而低密度脂蛋白受体mRNA表达没有变化。用佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）处理使HL-60细胞分化形成的巨噬细胞中，VLDL受体mRNA水平没有变化。用1α,25(OH)2D3处理具有维生素D受体的肉瘤细胞（MG-63细胞系）不影响VLDL受体mRNA水平。因此，1α,25(OH)2D3通过依赖分化的机制诱导HL-60细胞中VLDL受体mRNA的表达。
