Antithrombotic potential of a single-domain antibody enhancing the activated protein C-cofactor activity of protein S.


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:
07 2022
Historique:
revised: 05 04 2022
received: 23 11 2021
accepted: 19 04 2022
pubmed: 22 4 2022
medline: 29 6 2022
entrez: 21 4 2022
Statut: ppublish

Résumé

Protein S (PS) is a natural anticoagulant acting as a cofactor for activated protein C (APC) in the proteolytic inactivation of activated factors V (FVa) and VIII (FVIIIa), but also for tissue factor pathway inhibitor α (TFPIα) in the inhibition of activated factor X (FXa). For therapeutic purposes, we aimed at generating single-domain antibodies (sdAbs) that could specifically modulate the APC-cofactor activity of PS in vivo. A llama-derived immune library of sdAbs was generated and screened on recombinant human PS by phage display. PS binders were tested in a global activated partial thromboplastin time (APTT)-based APC-cofactor activity assay. A PS-specific sdAb (PS003) was found to enhance the APC-cofactor activity of PS in our APTT-based assay, and this enhancing effect was greater for a bivalent form of PS003 (PS003biv). Further characterization of PS003biv demonstrated that PS003biv also enhanced the APC-cofactor activity of PS in a tissue factor (TF)-induced thrombin generation assay and stimulated APC in the inactivation of FVa, but not FVIIIa, in plasma-based assays. Furthermore, PS003biv was directed against the sex hormone-binding globulin (SHBG)-like domain but did not inhibit the binding of PS to C4b-binding protein (C4BP) and did not interfere with the TFPIα-cofactor activity of PS. In mice, PS003biv exerted an antithrombotic effect in a FeCl Altogether, these results showed that pharmacological enhancement of the APC-cofactor activity of PS through an original anti-PS sdAb might constitute a promising and safe antithrombotic strategy.

Sections du résumé

BACKGROUND
Protein S (PS) is a natural anticoagulant acting as a cofactor for activated protein C (APC) in the proteolytic inactivation of activated factors V (FVa) and VIII (FVIIIa), but also for tissue factor pathway inhibitor α (TFPIα) in the inhibition of activated factor X (FXa).
OBJECTIVE
For therapeutic purposes, we aimed at generating single-domain antibodies (sdAbs) that could specifically modulate the APC-cofactor activity of PS in vivo.
METHODS
A llama-derived immune library of sdAbs was generated and screened on recombinant human PS by phage display. PS binders were tested in a global activated partial thromboplastin time (APTT)-based APC-cofactor activity assay.
RESULTS
A PS-specific sdAb (PS003) was found to enhance the APC-cofactor activity of PS in our APTT-based assay, and this enhancing effect was greater for a bivalent form of PS003 (PS003biv). Further characterization of PS003biv demonstrated that PS003biv also enhanced the APC-cofactor activity of PS in a tissue factor (TF)-induced thrombin generation assay and stimulated APC in the inactivation of FVa, but not FVIIIa, in plasma-based assays. Furthermore, PS003biv was directed against the sex hormone-binding globulin (SHBG)-like domain but did not inhibit the binding of PS to C4b-binding protein (C4BP) and did not interfere with the TFPIα-cofactor activity of PS. In mice, PS003biv exerted an antithrombotic effect in a FeCl
DISCUSSION
Altogether, these results showed that pharmacological enhancement of the APC-cofactor activity of PS through an original anti-PS sdAb might constitute a promising and safe antithrombotic strategy.

Identifiants

pubmed: 35445541
doi: 10.1111/jth.15736
pii: S1538-7836(22)01927-4
doi:

Substances chimiques

Fibrinolytic Agents 0
Protein C 0
Protein S 0
Single-Domain Antibodies 0
Factor VIIIa 72175-66-7

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1653-1664

Informations de copyright

© 2022 International Society on Thrombosis and Haemostasis.

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Auteurs

Josepha C Sedzro (JC)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.

Frédéric Adam (F)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.

Claire Auditeau (C)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
Service d'Hématologie Biologique, Hôpital Necker Enfants Malades, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.

Elsa Bianchini (E)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.

Allan De Carvalho (A)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.

Ivan Peyron (I)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.

Sadyo Daramé (S)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.

Sophie Gandrille (S)

Innovations Thérapeutiques en Hémostase, UMR-S1140, INSERM, Université de Paris, Paris, France.
Service d'Hématologie Biologique, Hôpital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.

Stella Thomassen (S)

Cardiovascular Research Institute Maastricht (CARIM), University Maastricht, Maastricht, the Netherlands.

Tilman M Hackeng (TM)

Cardiovascular Research Institute Maastricht (CARIM), University Maastricht, Maastricht, the Netherlands.

Olivier D Christophe (OD)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.

Peter J Lenting (PJ)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.

Cécile V Denis (CV)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.

Delphine Borgel (D)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
Service d'Hématologie Biologique, Hôpital Necker Enfants Malades, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.

François Saller (F)

Hémostase, Inflammation, Thrombose (HITh), UMR-S1176, INSERM, Université Paris-Saclay, Le Kremlin-Bicêtre, France.

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