Interleukin-1beta and interleukin-6 increase levels of apolipoprotein B mRNA and decrease accumulation of its protein in culture medium of HepG2 cells.

Interleukin-1beta and interleukin-6 increase levels of apolipoprotein B mRNA and decrease accumulation of its protein in culture medium of HepG2 cells.
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Interleukin-1beta 和 interleukin-6 增加 HepG2 细胞培养基中载脂蛋白 B mRNA 的水平并减少其蛋白质的积累。

DOI:
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发表时间:
1998
影响因子:
6.5
通讯作者:
Y. Maruyama
Y. Maruyama
中科院分区:
生物学2区
文献类型:
--
作者:
K. Yokoyama;T. Ishibashi;L. Yi;A. Nagayoshi;T. Teramoto;Y. Maruyama

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本研究旨在探讨细胞因子对HepG 2细胞载脂蛋白B(apoB)mRNA及其蛋白水平的调节作用。在单独存在白细胞介素-1 β(IL-1 β)或IL-6的情况下,观察到apoB mRNA水平呈剂量依赖性增加。这种增加早在IL-1 β或IL-6刺激后1小时就发生了。外源性添加IL-1 β(5 ng/ml)和IL-6(50 ng/ml)诱导的2.8和2.1倍的增加,作为18小时的培养结果,分别。与IL-1 β和IL-6的共刺激显著增强了单独使用任一细胞因子刺激的apoB mRNA水平的增加。放线菌酮治疗阻止IL-1 β诱导apoB mRNA,但不能阻止IL-6诱导apoB mRNA。这些发现表明,这些细胞因子通过不同的途径介导apoB mRNA水平的增强。相反,IL-1 β和IL-6降低了培养基中apoB蛋白水平的积累。脉冲追踪研究表明,与对照组相比,向培养基中加入N-乙酰亮氨酰亮氨酰正亮氨酸诱导细胞裂解物中新合成的apoB对IL-1 β(P < 0.05)或IL-6(不显著程度)的反应减少。这些结果表明,培养基中apoB水平较低是由细胞内降解增强引起的。此外,IL-1 β增加LDL受体mRNA水平以及蛋白活性,尽管IL-6没有,这表明与IL-6诱导的相比,IL-1 β诱导的培养基中apoB积累的更显著降低可能反映了IL-1 β从培养基中摄取apoB的增加。目前的研究表明,细胞因子网络可能涉及在某些条件下,如炎症的apoB的代谢。
The purpose of the present study was to examine the regulation of levels of apolipoprotein B (apoB) mRNA and its protein by cytokines in HepG2 cells. A dose-dependent increase in apoB mRNA levels was observed in the presence of either interleukin-1beta (IL-1beta) or IL-6 alone. This increase occurred as early as 1 h after IL-1beta or IL-6 stimulation. Exogenous addition of IL-1beta (5 ng/ml) and IL-6 (50 ng/ml) induced 2.8- and 2.1-fold increases as a result of 18 h of culture, respectively. Co-stimulation with IL-1beta and IL-6 significantly enhanced the increase in apoB mRNA levels stimulated with either cytokine alone. Treatment with cycloheximide prevented the induction of apoB mRNA by IL-1beta, but not by IL-6. These findings suggest that enhancement of apoB mRNA levels by these cytokines is mediated through different pathways. Conversely, IL-1beta and IL-6 lowered the accumulation of apoB protein levels in the culture medium. The pulse-chase study showed that addition of N-acetyl leucyl leucyl norleucinal to the medium induced a decrease in newly synthesized apoB in the cell lysate in response to IL-1beta (P < 0.05) or IL-6 (not to a significant extent) compared with control. These findings demonstrated that the lower level of apoB in the medium was caused by the enhanced intracellular degradation. In addition, IL-1beta increased LDL receptor mRNA levels as well as protein activity, although IL-6 did not, suggesting that the more marked decrease in apoB accumulation in the medium induced by IL-1beta compared with that induced by IL-6 may reflect an increased uptake of apoB from the medium by IL-1beta. The present study demonstrates that a cytokine network may be involved in the metabolism of apoB under certain conditions such as inflammation.
DOI: 10.1126/science.3513311
发表时间: 1986-04-04
期刊: SCIENCE
影响因子: 56.9
作者:
BROWN, MS;GOLDSTEIN, JL
通讯作者: GOLDSTEIN, JL
DOI: 10.1126/science.3010466
发表时间: 1986-06-06
期刊: SCIENCE
影响因子: 56.9
作者:
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载脂蛋白 B 和脂蛋白代谢。
DOI: 10.1016/b978-0-12-024921-3.50007-1
发表时间: 1985
期刊: Advances in lipid research
影响因子: --
作者:
Sparks,JD;Sparks,CE
通讯作者: Sparks,CE
DOI: 10.1161/01.atv.14.1.8
发表时间: 1994-01-01
期刊: ARTERIOSCLEROSIS AND THROMBOSIS
影响因子: --
作者:
ETTINGER, WH;VARMA, VK;VERDERY, PB
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DOI: --
发表时间: 1985
影响因子: 6.5
作者:
Grundy,SM;Vega,GL
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