Do electrostatic interactions determine glycation of hyaluronidase derivatives with N-acetylhexosamines?

被引:0
作者
Turashev A.D. [1 ]
Tischenko E.G. [1 ]
Maksimenko A.V. [1 ]
机构
[1] Institute of Experimental Cardiology, Russian Cardiology Research-and-Production Complex, Moscow, 121552
基金
俄罗斯基础研究基金会;
关键词
Chondroitin sulfate; Electrostatic interactions; Glycation; Hyaluronan fragments; Hyaluronidase; Ionic strength of medium; N-acetylhexosamines;
D O I
10.1134/S1990750812020151
中图分类号
学科分类号
摘要
Using N-acetylglucosamine and N-acetylgalactosamine as model agents for glycation of native hyaluronidase and its chondroitin sulfate modified form it has been shown that the modified enzyme exhibited higher inactivation than the native enzyme, while heparin caused similar inhibition of both forms. Such effect could be attributed to the development of electrostatic interactions as the modified hyaluronidase had altered surface electrostatic potential after chondroitin sulfate binding. However, variations in ionic strength of the medium containing enzyme derivatives have shown that their endoglycosidase activity changed in a similar manner and the effect on glycation represents a multifactor process. N-acetylhexosamines are natural labels of endothelial glycocalyx degradation products. Interaction of the hyaluronidase forms with charged hyaluronan fragments revealed significantly higher inactivation of the modified enzyme compared with the native enzyme. The glycation pattern observed in this study was opposite to that observed with mono- and disaccharides. Thus, it appears that the investigated hyaluronidase derivatives represent an informative enzymatic test in vivo for determination of the dominant type of glycation agents in blood circulation and their origin. © 2012 Pleiades Publishing, Ltd.
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页码:185 / 191
页数:6
相关论文
共 29 条
  • [1] Goldin A., Beckman J.A., Schmidt A.M., Creager M.A., Circulation, 114, pp. 597-605, (2006)
  • [2] Shapiro B.P., Owan T.E., Mohammed S.F., Meyer D.M., Mills L.D., Schalkwijk C.G., Redfield M.M., Circulation, 118, pp. 1002-1010, (2008)
  • [3] Zhang M., Kho A.L., Anilkumar N., Chibber R., Pagano P.J., Shah A.M., Cave A.C., Circulation, 113, pp. 1235-1243, (2006)
  • [4] McNulty M., Mahmud A., Feely J., Am. J. Hypertens., 20, pp. 242-247, (2007)
  • [5] Ge J., Jia Q., Liang C., Luo Y., Huang D., Sun A., Wang K., Zou Y., Chen H., Arterioscler. Thromb. Vasc. Biol., 25, pp. 2157-2163, (2005)
  • [6] Ceriello A., Motz E., Arterioscler. Thromb. Vasc. Biol., 24, pp. 816-823, (2004)
  • [7] Bucciarelli L.G., Kaneko M., Ananthakrishnan R., Harja E., Lee L.K., Hwang Y.C., Lerner S., Bakr S., Li Q., Lu Y., Song F., Qu W., Gomez T., Zou Y.S., Yan S.F., Schmidt A.M., Ramasamy R., Circulation, 113, pp. 1226-1234, (2006)
  • [8] Basta G., Atherosclerosis, 196, pp. 9-21, (2008)
  • [9] Maksimenko A.V., Schechilina Yu.V., Tischenko E.G., Biochemistry (Moscow), 68, pp. 1055-1062, (2003)
  • [10] Turashev A.D., Tischenko E.G., Maksimenko A.V., Mol. Med., 3, pp. 51-56, (2009)