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Cell biology

Mast-cell heparin demystified

Nature volume 400, pages 714–715 (1999)Cite this article

Although the clotting of blood (thrombosis) can be life-saving when it stops the bleeding associated with extensive trauma, in settings such as heart attack, stroke and pulmonary embolism, it can cause disease or even death1. For this reason, heparin — which can prevent or arrest clot formation2,3 — is one of medicine's most commonly used drugs. Yet its physiological importance has long been obscure.

Humphries et al.4 and Forsberg et al.5 now report (on pages 769 and 773 of this issue) that targeted disruption of the gene for glucosaminyl N-deacetylase/N-sulphotransferase-2 (NDST-2) produces transgenic mice that lack heparin, revealing a physiological function for this molecule. Heparin, it seems, regulates the types and amounts of other biologically active mediators in the cytoplasmic granules of a group of cells found in almost all tissues6,7. These cells — the mast cells — are effector cells of inflammation and immunity. So, by regulating the mediators in mast cells, heparin may influence the expression of inflammatory and immunological responses.

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Figure 1: Cell biology and functions of mast-cell heparin, based in part on the findings of Humphries et al.4 and Forsberg et al.5.

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Authors and Affiliations

  1. Stanford University School of Medicine, L235, 300 Pasteur Drive, Stanford, 94305-5324, California, USA

    James L. Zehnder & Stephen J. Galli

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  1. James L. Zehnder
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Zehnder, J., Galli, S. Mast-cell heparin demystified. Nature 400, 714–715 (1999). https://doi.org/10.1038/23360

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