Induction of beta 2-adrenergic receptor mRNA and ligand binding in HeLa cells.

R S Duman, P H Fishman, J F Tallman
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引用次数: 5

Abstract

HeLa cells express low levels of beta-adrenergic receptor (beta AR) of the beta 2-subtype. When exposed to sodium butyrate, receptor levels increased up to 4-fold in a time dependent manner, reaching a maximum after 12 to 15 h of treatment. Sodium butyrate treatment also caused a 3 to 4 fold increase in levels of beta 2AR mRNA determined by hybridization blot analysis. The induction of beta 2AR mRNA temporally preceded the increase in receptor binding activity, reaching a maximum after 4 to 6 h of treatment, and remaining elevated for up to 24 h. Prior exposure of the cells to the protein synthesis inhibitor cycloheximide prevented the butyrate-induced increase in receptor binding but had no effect on the increase in receptor mRNA. Blocking DNA synthesis and cell growth by excess thymidine did not increase beta 2AR mRNA or binding or prevent the effects of sodium butyrate. Thus, butyrate appears to induce beta 2AR mRNA by a mechanism independent of DNA and protein synthesis.

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β 2-肾上腺素能受体mRNA与配体结合在HeLa细胞中的诱导作用。
HeLa细胞表达低水平的β 2亚型β肾上腺素能受体(β AR)。当暴露于丁酸钠时,受体水平以时间依赖性的方式增加了4倍,在处理12至15小时后达到最大值。通过杂交印迹分析,丁酸钠处理也导致β 2AR mRNA水平增加3至4倍。β 2AR mRNA的诱导暂时领先于受体结合活性的增加,在处理4至6小时后达到最大值,并保持升高长达24小时。先前暴露于蛋白质合成抑制剂环己亚胺的细胞阻止了丁酸盐诱导的受体结合增加,但对受体mRNA的增加没有影响。过量胸腺嘧啶阻断DNA合成和细胞生长不会增加β 2AR mRNA或结合,也不会阻止丁酸钠的作用。因此,丁酸盐似乎通过一种独立于DNA和蛋白质合成的机制诱导β 2AR mRNA。
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