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人肝癌细胞中的急性期蛋白合成:白细胞介素-1和白细胞介素-6对血清淀粉样蛋白A(SAA)和触珠蛋白的差异调节

Acute-phase protein synthesis in human hepatoma cells: differential regulation of serum amyloid A (SAA) and haptoglobin by interleukin-1 and interleukin-6.

作者信息

Raynes J G, Eagling S, McAdam K P

机构信息

Department of Clinical Sciences, London School of Hygiene and Tropical Medicine, England.

出版信息

Clin Exp Immunol. 1991 Mar;83(3):488-91. doi: 10.1111/j.1365-2249.1991.tb05666.x.

DOI:10.1111/j.1365-2249.1991.tb05666.x
PMID:1706240
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1535311/
Abstract

Interleukin-6 (IL-6, BSF-2 or IFN-beta 2) is thought to be the major regulator of the acute-phase protein response that follows tissue injury and inflammation, with interleukin-1 (IL-1), tumour necrosis factor and more recently, LIF or HSF III, slightly stimulatory on only certain acute phase proteins. The synthesis of the major acute-phase protein SAA, originally described as being synthesized in response to IL-1, has been claimed recently to be mainly under IL-6 regulation. Our results show that in the human hepatoma cell line HuH-7, IL-1 is the major stimulating cytokine increasing SAA synthesis by a factor in excess of 100-fold. We also show that under most conditions interleukin-6 and tumour necrosis factor stimulate additively in combination with IL-1. Isoelectric focusing has demonstrated that SAA1 and SAA2 alpha are expressed but not SAA2 beta. The HuH-7 cell line is IL-6 responsive since haptoglobin is stimulated mainly by IL-6.

摘要

白细胞介素-6(IL-6,即BSF-2或IFN-β2)被认为是组织损伤和炎症后急性期蛋白反应的主要调节因子,白细胞介素-1(IL-1)、肿瘤坏死因子,以及最近发现的白血病抑制因子(LIF)或热休克因子III(HSF III),仅对某些急性期蛋白有轻微刺激作用。主要急性期蛋白血清淀粉样蛋白A(SAA)最初被描述为在IL-1作用下合成,最近有人声称其合成主要受IL-6调控。我们的结果表明,在人肝癌细胞系HuH-7中,IL-1是增加SAA合成的主要刺激细胞因子,其增加幅度超过100倍。我们还表明,在大多数情况下,白细胞介素-6和肿瘤坏死因子与IL-1联合刺激具有相加作用。等电聚焦显示表达了SAA1和SAA2α,但未表达SAA2β。HuH-7细胞系对IL-6有反应,因为触珠蛋白主要受IL-6刺激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0684/1535311/081ed7cb6c80/clinexpimmunol00066-0148-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0684/1535311/081ed7cb6c80/clinexpimmunol00066-0148-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0684/1535311/081ed7cb6c80/clinexpimmunol00066-0148-a.jpg

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