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Glycobiology. 2009 May;19(5):479-87. doi: 10.1093/glycob/cwp003. Epub 2009 Jan 15.

Molecular insights into beta-galactoside alpha2,6-sialyltransferase secretion in vivo.

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Glyco-chain Functions Laboratory, RIKEN, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan.


Beta-galactoside alpha2,6-sialyltransferase (ST6Gal I), which is highly expressed in the liver, is mainly cleaved by Alzheimer's beta-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.

[Indexed for MEDLINE]

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