Activation mechanism dependent surface exposure of cellular factor XIII on activated platelets and platelet microparticles.
cell-derived microparticles
factor XIII
flow cytometry
immune electron microscopy
platelet activation
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:
05 2022
05 2022
Historique:
received:
08
07
2021
accepted:
04
02
2022
pubmed:
12
2
2022
medline:
23
4
2022
entrez:
11
2
2022
Statut:
ppublish
Résumé
Platelets contain a high amount of potentially active A subunit dimer of coagulation factor XIII (cellular FXIII; cFXIII). It is of cytoplasmic localization, not secreted, but becomes translocated to the surface of platelets activated by convulxin and thrombin (CVX+Thr). To explore the difference in cFXIII translocation between receptor mediated and non-receptor mediated platelet activation and if translocation can also be detected on platelet-derived microparticles. Our aim was also to shed some light on the mechanism of cFXIII translocation. Gel-filtered platelets were activated by CVX+Thr or Ca Receptor mediated activation by CVX+Thr exposed cFXIII to the surface of more than 60% of platelets. Electron microscopy revealed microparticles with preserved membrane structure and microparticles devoid of labeling for membrane glycoprotein CD41a. cFXIII was observed on both types of microparticles but was more abundant in the absence of CD41a. Rhosin, a RhoA inhibitor, significantly decreased cFXIII translocation. Non-receptor mediated activation of platelets by calcimycin elevated intracellular Ca The elevation of intracellular Ca
Sections du résumé
BACKGROUND
Platelets contain a high amount of potentially active A subunit dimer of coagulation factor XIII (cellular FXIII; cFXIII). It is of cytoplasmic localization, not secreted, but becomes translocated to the surface of platelets activated by convulxin and thrombin (CVX+Thr).
OBJECTIVE
To explore the difference in cFXIII translocation between receptor mediated and non-receptor mediated platelet activation and if translocation can also be detected on platelet-derived microparticles. Our aim was also to shed some light on the mechanism of cFXIII translocation.
METHODS
Gel-filtered platelets were activated by CVX+Thr or Ca
RESULTS
Receptor mediated activation by CVX+Thr exposed cFXIII to the surface of more than 60% of platelets. Electron microscopy revealed microparticles with preserved membrane structure and microparticles devoid of labeling for membrane glycoprotein CD41a. cFXIII was observed on both types of microparticles but was more abundant in the absence of CD41a. Rhosin, a RhoA inhibitor, significantly decreased cFXIII translocation. Non-receptor mediated activation of platelets by calcimycin elevated intracellular Ca
CONCLUSIONS
The elevation of intracellular Ca
Identifiants
pubmed: 35146910
doi: 10.1111/jth.15668
pmc: PMC9303193
pii: S1538-7836(22)00160-X
doi:
Substances chimiques
Carrier Proteins
0
Phosphatidylserines
0
Calcimycin
37H9VM9WZL
Factor XIII
9013-56-3
Thrombin
EC 3.4.21.5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1223-1235Subventions
Organisme : British Heart Foundation
ID : PG/07/122/24195
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/11/1/28461
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/11/2/28579
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/20/17/35050
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/15/82/31721
Pays : United Kingdom
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2022 The Authors. Journal of Thrombosis and Haemostasis published by Wiley Periodicals LLC on behalf of International Society on Thrombosis and Haemostasis.
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