Regulation of haptoglobin gene expression in 3T3-L1 adipocytes by cytokines, catecholamines, and PPARγ

Regulation of haptoglobin gene expression in 3T3-L1 adipocytes by cytokines, catecholamines, and PPARγ
复制标题

DOI:
10.1016/j.bbrc.2003.12.008
复制
发表时间:
2004-01-16
影响因子:
3.1
通讯作者:
Trayhurn, P
Trayhurn, P
中科院分区:
生物学4区
文献类型:
--
作者:
do Nascimento, CO;Hunter, L;Trayhurn, P

文献摘要

被引文献

相似文献

已经使用 3T3-L1 细胞检查了调节脂肪细胞中触珠蛋白(急性期反应物)基因表达的因素。通过Northern印迹法在小鼠的每个主要白色脂肪组织库(附睾、皮下、肠系膜和肾周)和肩胛间棕色脂肪中观察到触珠蛋白表达。表达发生在成熟脂肪细胞中,但不在基质血管部分中。在3T3-L1细胞中,从诱导分化为脂肪细胞后第4天开始检测到触珠蛋白mRNA。脂多糖和细胞因子、TNFα 和白细胞介素 6 导致 3T3-L1 脂肪细胞中触珠蛋白 mRNA 大幅增加; TNFα 的增幅最高(7 倍)。地塞米松、去甲肾上腺素、异丙肾上腺素和 β3-肾上腺素受体激动剂也可诱导触珠蛋白 mRNA 水平的增加。相反,烟酸和 PPARγ 激动剂罗格列酮可减少触珠蛋白 mRNA。 RT-PCR显示触珠蛋白基因在人脂肪组织(皮下、网膜)中表达。结论是脂肪细胞中触珠蛋白基因的表达受到炎症细胞因子、糖皮质激素和交感系统的刺激,而PPARγ核受体的激活具有强烈的抑制作用。 (C) 2003 Elsevier Inc. 保留所有权利。
Factors which regulate expression of the haptoglobin (acute phase reactant) gene in adipocytes have been examined using 3T3-L1 cells. Haptoglobin expression was observed by Northern blotting in each of the major white adipose tissue depots of mice (epididymal, subcutaneous, mesenteric, and perirenal) and in interscapular brown fat. Expression occurred in mature adipocytes, but not in the stromal-vascular fraction. In 3T3-L1 cells, haptoglobin mRNA was detected from day 4 after the induction of differentiation into adipocytes. Lipopolysaccharide and the cytokines, TNFalpha and interleukin-6, resulted in substantial increases in haptoglobin mRNA in 3T3-L1 adipocytes; the increase (7-fold) was highest with TNFalpha. Increases in haptoglobin mRNA level were also induced by dexamethasone, noradrenaline, isoprenaline, and a beta3-adrenoceptor agonist. In contrast, haptoglobin mRNA was reduced by nicotinic acid and the PPARgamma agonist, rosiglitazone. RT-PCR showed that the haptoglobin gene was expressed in human adipose tissue (subcutaneous, omental). It is concluded that haptoglobin gene expression in adipocytes is stimulated by inflammatory cytokines, glucocorticoids, and the sympathetic system, while activation of the PPARgamma nuclear receptor is strongly inhibitory. (C) 2003 Elsevier Inc. All rights reserved.