Protection by recombinant alpha 1-antitrypsin Ala357 Arg358 against arterial hypotension induced by factor XII fragment.

Details

Serval ID
serval:BIB_89B0B5E9BBC1
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Protection by recombinant alpha 1-antitrypsin Ala357 Arg358 against arterial hypotension induced by factor XII fragment.
Journal
The Journal of clinical investigation
Author(s)
Schapira M., Ramus M.A., Waeber B., Brunner H.R., Jallat S., Carvallo D., Roitsch C., Courtney M.
ISSN
0021-9738 (Print)
ISSN-L
0021-9738
Publication state
Published
Issued date
08/1987
Peer-reviewed
Oui
Volume
80
Number
2
Pages
582-585
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
The specificity of serpin superfamily protease inhibitors such as alpha 1-antitrypsin or C1 inhibitor is determined by the amino acid residues of the inhibitor reactive center. To obtain an inhibitor that would be specific for the plasma kallikrein-kinin system enzymes, we have constructed an antitrypsin mutant having Arg at the reactive center P1 residue (position 358) and Ala at residue P2 (position 357). These modifications were made because C1 inhibitor, the major natural inhibitor of kallikrein and Factor XIIa, contains Arg at P1 and Ala at P2. In vitro, the novel inhibitor, alpha 1-antitrypsin Ala357 Arg358, was more efficient than C1 inhibitor for inhibiting kallikrein. Furthermore, Wistar rats pretreated with alpha 1-antitrypsin Ala357 Arg358 were partially protected from the circulatory collapse caused by the administration of beta-Factor XIIa.
Keywords
Animals, Blood Coagulation, Complement C1 Inactivator Proteins/metabolism, Factor XII/antagonists & inhibitors, Hypotension/prevention & control, Kallikreins/metabolism, Kinetics, Prekallikrein/metabolism, Rats, Recombinant Proteins, Thrombin/metabolism, Thrombin Time, alpha 1-Antitrypsin/analogs & derivatives, alpha 1-Antitrypsin/pharmacology
Pubmed
Web of science
Open Access
Yes
Create date
25/01/2008 15:27
Last modification date
24/02/2024 7:33
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