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The short loop between epidermal growth factor-like domains 4 and 5 is critical for human thrombomodulin function
J H Clarke1, D R Light, E Blasko
1Department of Protein Chemistry, Berlex Biosciences, Richmond, California 94804.
Abstract:
Thrombomodulin (TM) is a cofactor for activation of protein C by thrombin. We showed that 80-90% of this cofactor activity is lost by oxidation of Met388, located within the short interdomain loop between epidermal growth factor-like domains 4 and 5 (Glaser, C. B., Morser, J., Clarke, J. H., Blasko, E., McLean, K., Kuhn, I., Chang, R.-J., Lin, J.-H., Vilander, L., Andrews, W. H., and Light, D. R. (1992) J. Clin. Invest. 90, 2565-2573). For each of the 3 amino acids of the loop, site-specific mutants are described in which, 1) all possible single amino acid substitutions are made, 2) deletions are made, or 3) alanine is inserted adjacent to each residue of the loop. Most substitutions within the loop (38/57) result in a > 50% decrease in cofactor activity, while changes in the length of this region result in > 90% loss of activity. Only the Met388-->Leu mutant has higher cofactor activity (2-fold) than wild-type TM. A number of soluble and full-length TM analogs with the Met388-->Leu substitution are improved thrombin cofactors, whether produced in bacteria, insect, or mammalian cells. Detailed kinetic analysis of a soluble TM analog consisting of the six EGF-like domains secreted from insect cells shows that the enhanced activity of the Met388-->Leu mutant results from an increased catalytic efficiency (kcat/Km). This enhancement is maximal at physiological concentrations of calcium. The loss of activity following Met388 oxidation in the wild-type protein is the result of both decreased binding to thrombin (Kd effect) and a decreased interaction of the TM.thrombin complex with protein C (Km effect). We demonstrate the critical role of this interdomain loop in the biological anticoagulant properties of TM.
Insights
Thrombomodulin
Area of Science:
- Biochemistry
- Molecular Biology
- Protein Engineering
Background:
- Thrombomodulin (TM) is a crucial cofactor for thrombin-mediated protein C activation.
- Oxidation of methionine 388 (Met388) in TM significantly reduces its cofactor activity.
- The interdomain loop between EGF-like domains 4 and 5 is critical for TM function.
Purpose of the Study:
- To investigate the role of the interdomain loop in TM cofactor activity.
- To identify specific mutations that enhance TM anticoagulant properties.
- To elucidate the mechanisms underlying TM activity loss upon Met388 oxidation.
Main Methods:
- Site-directed mutagenesis of the TM interdomain loop, including substitutions, deletions, and alanine insertions.
- Expression and purification of wild-type and mutant TM analogs in various cell systems (bacteria, insect, mammalian).
- Kinetic analysis (kcat/Km, Kd) of TM-thrombin-protein C interactions, with a focus on calcium dependence.
Main Results:
- Most loop mutations (>50%) decreased TM cofactor activity by over 50%.
- Mutations altering loop length resulted in >90% activity loss.
- The Met388 to Leucine (Met388-->Leu) substitution yielded a 2-fold increase in cofactor activity.
- Met388-->Leu TM analogs exhibited enhanced catalytic efficiency (kcat/Km), particularly at physiological calcium levels.
- Met388 oxidation impairs TM function by reducing thrombin binding (Kd) and TM-thrombin complex interaction with protein C (Km).
Conclusions:
- The interdomain loop, particularly Met388, is essential for TM's anticoagulant function.
- The Met388-->Leu mutation significantly enhances TM cofactor activity through improved catalytic efficiency.
- Targeted mutagenesis of the TM interdomain loop offers a strategy to improve anticoagulant properties.