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Gut 2000;47:14-15; doi:10.1136/gut.47.1.14
Copyright © 2000 BMJ Publishing Group Ltd & British Society of Gastroenterology.
Gut 2000;47:14-15 ( July )

Commentary

See article on page 88

Heparin and inflammation: a new use for an old GAG?

The first 150 words of the full text of this article appear below.

Since its discovery in 1917, heparin has been a fascinating, and in a way elusive, molecule. Heparin is a glycosoaminoglycan (GAG) formed by repeated sulphated oligosaccharide units. Natural preparations of heparin (usually obtained from bovine lung or porcine intestinal mucosa) can vary in the length of the polymeric unit and therefore have different molecular weights. As such, the biological actions of this GAG can vary quantitatively between different batches of the molecule. The initial activity ascribed to heparin was its capacity to prolong the process of blood clotting, an effect due to its potentiating interaction with the natural inhibitor of thrombin, antithrombin III. These properties have led to widespread use of heparin as an anticoagulant although scant attention has been paid to other biological activities of this GAG.

This situation has changed in recent years. In fact is has long been recognised that heparin has a wide range of biological effects . . . [Full text of this article]


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Relevant Article

Heparin attenuates TNF-alpha induced inflammatory response through a CD11b dependent mechanism
A Salas, M Sans, A Soriano, J C Reverter, D C Anderson, J M Piqué, and J Panés
Gut 2000 47: 88-96. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

  • Christopherson, K. W. II, Campbell, J. J., Travers, J. B., Hromas, R. A. (2002). Low-Molecular-Weight Heparins Inhibit CCL21-Induced T Cell Adhesion and Migration. J. Pharmacol. Exp. Ther. 302: 290-295 [Abstract] [Full Text]  

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