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J. Biol. Chem., Vol. 266, Issue 23, 15356-15362, 08, 1991
KJ Frommherz, B Faller and JG Bieth
Heparin depresses the second-order rate constant ka for the inhibition of
neutrophil elastase by alpha 1-proteinase inhibitor. High molecular mass
heparin decreases ka from 1.3 x 10(7) M-1 s-1 to a limit of 4.6 x 10(4) M-1
s-1. Low molecular mass heparin is about 7-fold less effective. Dermatan
sulfate and chondroitin sulfate are less efficient. Heparin preparations
used in clinical care also strongly depress ka when tested at
concentrations corresponding to their clinical efficacy. Heparin also
decreases the ka for the elastase/eglin c and the cathepsin G/alpha
1-proteinase inhibitor systems but not that for the alpha 1-proteinase
inhibitor/pancreatic elastase or trypsin pairs. These results, together
with Sepharose-heparin binding studies, indicate that the ka-depressing
effect of the polymer is related to its ability to form a tight complex
with elastase but not with alpha 1- proteinase inhibitor. One mol of high
molecular mass heparin binds 3 mol of neutrophil elastase with a Kd of 3.3
nM. Low molecular mass heparin binds elastase with a 1:1 stoichiometry and
a Kd of 89 nM. For both heparins ka is lowest when elastase is fully
saturated with heparin. From this we conclude that heparin decreases ka,
because the heparin-elastase complex is able to slowly react with alpha 1-
proteinase inhibitor and not because the inhibitor slowly dissociates the
heparin-elastase complex. These findings may have important
pathophysiological bearing.
Heparin strongly decreases the rate of inhibition of neutrophil elastase by alpha 1-proteinase inhibitor
Laboratoire d'Enzymologie, Institut National de la Sante et de la Recherche Medicale U 237, Universite Louis Pasteur de Strasbourg, Illkirch, France.
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