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Glycobiology Advance Access originally published online on January 15, 2009
Glycobiology 2009 19(5):479-487; doi:10.1093/glycob/cwp003
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© The Author 2009. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Molecular insights into β-galactoside {alpha}2,6-sialyltransferase secretion in vivo

Shinobu Kitazume1,2,4,5, Ritsuko Oka4,5, Kazuko Ogawa4,5, Satoshi Futakawa3,4,5, Yoshiaki Hagiwara6, Hajime Takikawa7, Michio Kato8, Akinori Kasahara9, Eiji Miyoshi10, Naoyuki Taniguchi2,11 and Yasuhiro Hashimoto3,4,5

4 Glyco-chain Functions Laboratory, RIKEN, 2-1 Hirosawa, Wako-shi, Saitama 351-0198
5 CREST, Japan Science and Technology Agency, Kawaguchi, Saitama 560-0082
6 Department of Biological Sciences, Immuno-Biological Laboratories, 1091-1 Naka, Fujioka-shi, Gunma 375-0005
7 Department of Medicine, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi, Tokyo 173-8605
8 Department of Gastroenterology, Osaka National Hospital, 2-1-14, Ho-enzaka, Chu-oku, Osaka 540-0006
9 Department of General Medicine, 2-2 Yamada-oka, Suita
10 Department of Molecular Biochemistry and Clinical Investigation
11 Department of Biochemistry, Osaka University Graduate School of Medicine, 1-7, Yamada-Oka, Osaka 565-0871, Japan

1 To whom correspondence should be addressed: Tel: +81-48-467-9616; Fax: +81-48-467-9617; e-mail: shinobuk{at}riken.jp

Received on November 12, 2008; revised on December 15, 2008; accepted on January 6, 2009

β-Galactoside {alpha}2,6-sialyltransferase (ST6Gal I), which is highly expressed in the liver, is mainly cleaved by Alzheimer's β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) and secreted into the serum. During our studies to elucidate the molecular mechanism underlying the cleavage and secretion of ST6Gal I, we hypothesized that plasma ST6Gal I may represent a sensitive biomarker for hepatopathological situations. In the present study, we used recently developed sandwich ELISA systems that specifically detect the soluble cleaved form of ST6Gal I in plasma. We found that the level of plasma ST6Gal I was increased in two different types of liver injury models. In zone 1 hepatocyte-injured rats, the level of plasma ST6Gal I was increased together with acute phase reactions. Meanwhile, in zone 3 hepatocyte-injured rats, ST6Gal I secretion was most likely triggered by oxidative stress. Taken together, we propose two possible mechanisms for the upregulation of plasma ST6Gal I in hepatopathological situations: one accompanied by acute phase reactions to increase hepatic ST6Gal I expression and the other triggered by oxidative stress in the liver. We also found that the serum level of ST6Gal I in hepatitis C patients was correlated with the activity of hepatic inflammation.

Key words: acute phasereaction / BACE1 / hepatitis / secretion / ST6Gal I

2 Present address: Disease Glycomics Team, RIKEN Advanced Science Institute, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan.

3 Present address: School of Medicine, Department of Biochemistry, Fukushima Medical University, Hikarigaoka-1, Fukushima-shi, Fukushima 960-1295, Japan.


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