Factor XIIIa-dependent retention of red blood cells in clots is mediated by fibrin α-chain crosslinking

Author:

Byrnes James R.1,Duval Cédric2,Wang Yiming3,Hansen Caroline E.456,Ahn Byungwook456,Mooberry Micah J.7,Clark Martha A.8,Johnsen Jill M.910,Lord Susan T.1,Lam Wilbur A.456,Meijers Joost C. M.1112,Ni Heyu3,Ariëns Robert A. S.2,Wolberg Alisa S.1ORCID

Affiliation:

1. Department of Pathology and Laboratory Medicine and McAllister Heart Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC;

2. Division of Cardiovascular and Diabetes Research, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom;

3. Canadian Blood Services, and Department of Laboratory Medicine and Pathobiology, St. Michael's Hospital, University of Toronto, Toronto, Canada;

4. School of Chemistry and Biochemistry, Georgia Institute of Technology, Atlanta, GA;

5. Wallace C. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA;

6. Aflac Cancer and Blood Disorders Center, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA;

7. Department of Medicine and

8. Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC;

9. Research Institute, Bloodworks Northwest, Seattle, WA;

10. Department of Medicine, University of Washington, Seattle, WA;

11. Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; and

12. Department of Plasma Proteins, Sanquin Research, Amsterdam, The Netherlands

Abstract

Key Points In the absence of FXIIIa activity, red blood cells are extruded from clots during clot contraction. Factor XIIIa promotes red blood cell retention in contracting clots by crosslinking fibrin α-chains.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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