A non-circulating pool of factor XI associated with glycosaminoglycans in mice.
Animals
Binding Sites
Carotid Artery Thrombosis
/ blood
Chlorides
/ toxicity
Endothelium, Vascular
/ metabolism
Factor XI
/ chemistry
Factor XI Deficiency
/ blood
Ferric Compounds
/ toxicity
Glycosaminoglycans
/ blood
Heparin
/ pharmacology
Humans
Kininogens
/ blood
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Models, Molecular
Papio
Prekallikrein
/ metabolism
Protein Binding
Protein Conformation
Rats
Rats, Sprague-Dawley
Recombinant Proteins
/ metabolism
Sequence Alignment
Species Specificity
Static Electricity
factor XI
glycosaminoglycans
heparin
mice
protamine
Journal
Journal of thrombosis and haemostasis : JTH
ISSN: 1538-7836
Titre abrégé: J Thromb Haemost
Pays: England
ID NLM: 101170508
Informations de publication
Date de publication:
09 2019
09 2019
Historique:
received:
09
12
2018
accepted:
20
05
2019
pubmed:
28
5
2019
medline:
21
8
2020
entrez:
25
5
2019
Statut:
ppublish
Résumé
The homologous plasma proteins prekallikrein and factor XI (FXI) circulate as complexes with high molecular weight kininogen. Although evidence supports an interaction between the prekallikrein-kininogen complexes and vascular endothelium, there is conflicting information regarding FXI binding to endothelium. To study the interaction between FXI and blood vessels in mice. C57Bl/6 wild-type or F11-/- mice in which variants of FXI were expressed by hydrodynamic tail vein injection, received intravenous infusions of saline, heparin, polyphosphates, protamine, or enzymes that digest glycosaminoglycans (GAGs). Blood was collected after infusion and plasma was analyzed by western blot for FXI. Plasma FXI increased 5- to 10-fold in wild-type mice after infusion of heparin, polyphosphates, protamine, or GAG-digesting enzymes, but not saline. Similar treatments resulted in a much smaller change in plasma FXI levels in rats, and infusions of large boluses of heparin did not change FXI levels appreciably in baboons or humans. The releasable FXI fraction was reconstituted in F11-/- mice by expressing murine FXI, but not human FXI. We identified a cluster of basic residues on the apple 4 domain of mouse FXI that is not present in other species. Replacing the basic residues with alanine prevented the interaction of mouse FXI with blood vessels, whereas introducing the basic residues into human FXI allowed it to bind to blood vessels. Most FXI in mice is noncovalently associated with GAGs on blood vessel endothelium and does not circulate in plasma.
Sections du résumé
BACKGROUND
The homologous plasma proteins prekallikrein and factor XI (FXI) circulate as complexes with high molecular weight kininogen. Although evidence supports an interaction between the prekallikrein-kininogen complexes and vascular endothelium, there is conflicting information regarding FXI binding to endothelium.
OBJECTIVE
To study the interaction between FXI and blood vessels in mice.
METHODS
C57Bl/6 wild-type or F11-/- mice in which variants of FXI were expressed by hydrodynamic tail vein injection, received intravenous infusions of saline, heparin, polyphosphates, protamine, or enzymes that digest glycosaminoglycans (GAGs). Blood was collected after infusion and plasma was analyzed by western blot for FXI.
RESULTS AND CONCLUSIONS
Plasma FXI increased 5- to 10-fold in wild-type mice after infusion of heparin, polyphosphates, protamine, or GAG-digesting enzymes, but not saline. Similar treatments resulted in a much smaller change in plasma FXI levels in rats, and infusions of large boluses of heparin did not change FXI levels appreciably in baboons or humans. The releasable FXI fraction was reconstituted in F11-/- mice by expressing murine FXI, but not human FXI. We identified a cluster of basic residues on the apple 4 domain of mouse FXI that is not present in other species. Replacing the basic residues with alanine prevented the interaction of mouse FXI with blood vessels, whereas introducing the basic residues into human FXI allowed it to bind to blood vessels. Most FXI in mice is noncovalently associated with GAGs on blood vessel endothelium and does not circulate in plasma.
Identifiants
pubmed: 31125187
doi: 10.1111/jth.14494
pmc: PMC6768408
mid: NIHMS1051731
pii: S1538-7836(22)14140-1
doi:
Substances chimiques
Chlorides
0
Ferric Compounds
0
Glycosaminoglycans
0
Kininogens
0
Recombinant Proteins
0
Heparin
9005-49-6
Factor XI
9013-55-2
Prekallikrein
9055-02-1
ferric chloride
U38V3ZVV3V
Types de publication
Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1449-1460Subventions
Organisme : British Heart Foundation
ID : RG/12/9/29775
Pays : United Kingdom
Organisme : NHLBI NIH HHS
ID : R01 HL130018
Pays : United States
Organisme : American Heart Association-American Stroke Association
ID : 18POST34030076
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM116184
Pays : United States
Organisme : NHLBI NIH HHS
ID : R35 HL140025
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL081326
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL058837
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK020593
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL101972
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2019 International Society on Thrombosis and Haemostasis.
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