Inflammation-dependent changes in α2,3-, α2,6-, and α2,8-sialic acid glycotopes on serum glycoproteins in mice
Inflammation-dependent changes in α2,3-, α2,6-, and α2,8-sialic acid glycotopes on serum glycoproteins in mice
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DOI：
10.1093/glycob/cwi068
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发表时间：
2005-09
期刊：
影响因子：
4.3
通讯作者：
Zenta Yasukawa;C. Sato;K. Kitajima
中科院分区：
文献类型：
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作者：
Zenta Yasukawa;C. Sato;K. Kitajima
急性期血清蛋白的表达增加，以响应炎症刺激。这些蛋白质中的大多数是糖蛋白，通常含有唾液酸（Sia）。然而，尚不清楚Sia在这些糖蛋白中的表达在炎症过程中如何变化。这项研究证明了血清糖蛋白上的[α] 2，3-、[α] 2，6-和[α] 2，8-Sia糖表位响应于松节油诱导的炎症的变化，基于凝集素和免疫印迹分析，通过使用唾液酸连接特异性凝集素，Maackia amurensis用于[α] 2，3-Sia糖表位，Sambucus sieboldiana用于[α] 2，6-Sia糖表位，和识别[α] 2，8-Neu 5Gc残基的二聚体和寡聚体的单克隆抗体2- 4 B（mAb.2- 4 B）。含有[α] 2，3-、[α] 2，6-或[α] 2，8-Sia糖表位的唾液酸糖蛋白数量有限。逆转录-聚合酶链反应（RT-PCR）分析炎症期间小鼠肝脏中已知唾液酸转移酶的mRNA表达谱，表明{szligbeta}-半乳糖苷[α] 2，3-唾液酸转移酶的表达上调（ST 3 Gal I和ST 3 Gal III）和{szligbeta}-N-乙酰半乳糖胺[alpha] 2，6-唾液酸转移酶（ST 6 GalNAc VI）以及{szligbeta}-半乳糖苷[α] 2，6-唾液酸转移酶（ST 6 Gal I）mRNA。值得注意的是，ST 3Gal I和III以及ST 6 GalNAc VI参与O-聚糖链上和可能神经节苷脂上的[α] 2，3-和[α] 2，6-Sia糖表位的合成，而ST 6 Gal I特异于N-聚糖链。这些结果为炎症诱导血清糖蛋白中唾液酸糖表位的表达提供了证据。我们证明，炎症显着增加了一个未知的32 kDa的糖蛋白的表达含有[α] 2，8-Sia糖表位。炎症小鼠血清中糖蛋白增加的机制仍有待研究，因为所有[α] 2，8-唾液酸转移酶（ST 8 Sia I-VI）的mRNA表达在炎症期间未发生变化。
The expression of acute-phase serum proteins increases in response to inflammatory stimuli. Most of these proteins are glycoproteins that often contain sialic acids (Sia). It is unknown, however, how the expression of Sia in these glycoproteins changes during inflammation. This study demonstrates changes in the [alpha]2,3-, [alpha]2,6-, and [alpha]2,8-Sia glycotopes on serum glycoproteins in response to turpentine oil-induced inflammation, based on lectin- and immunoblot analyses by using sialyl linkage-specific lectins, Maackia amurensis for the [alpha]2,3-Sia glycotope and Sambucus sieboldiana for the [alpha]2,6-Sia glycotopes, and monoclonal antibody 2-4B (mAb.2-4B) recognizing the di- and oligomers of the [alpha]2,8-Neu5Gc residue. There was an increase in a limited number of sialoglycoproteins containing the [alpha]2,3-, [alpha]2,6-, or [alpha]2,8-Sia glycotopes. Reverse transcription-polymerase chain reaction (RT-PCR) analysis of the expression profiles of mRNAs for the known sialyltransferases in mouse liver during inflammation indicated the up-regulated expression of {szligbeta}-galactoside [alpha]2,3-sialyltransferases (ST3Gal I and ST3Gal III) and {szligbeta}-N-acetylgalactosaminide [alpha]2,6-sialyltransferase (ST6GalNAc VI) as well as {szligbeta}-galactoside [alpha]2,6-sialyltransferase (ST6Gal I) mRNAs. Notably, ST3Gal I and III and ST6GalNAc VI are involved in the synthesis of the [alpha]2,3- and [alpha]2,6-Sia glycotopes on O-glycan chains and possibly on gangliosides, whereas ST6Gal I is specific for N-glycan chains. These results provide evidence for the inflammation-induced expression of sialyl glycotopes in serum glycoproteins. We demonstrated that inflammation significantly increased the expression of an unknown 32-kDa glycoprotein containing the [alpha]2,8-Sia glycotope. The mechanism for the increase in glycoprotein in inflamed mouse serum remains to be examined, as mRNA expression for all of the [alpha]2,8-sialyltransferases (ST8Sia I-VI) was unchanged during inflammation.