Abstract Number: PB1848
Meeting: ISTH 2020 Congress
Theme: Role of Hemostatic System in Cancer, Inflammation and Immunity » Platelets and Inflammation
Background: Numerous autophagy proteinic components such as Beclin1, ATG7, ATG12-5 and LC3a/b are not only present but also modulated in platelets following stress, activation or starvation. Autophagy mechanisms are essential to the integrity of platelet functions. Platelet storage lesions (collection, processing, and storage) are considered as stress signals.
Aims: Our objective was to assess the impact that the Pathogen Inactivation (PI) procedure for platelet concentrates (PC) has on storage lesions and more specifically on autophagy and platelet functionality.
Methods: In order to do so, we evaluated both the importance and the evolution of autophagy biomarkers on PC. Autophagy was indirectly measured by the levels of LC3a/b, ATG5, SQSTM1, analysed by Western Blot i) on platelet-rich plasma (PRP) lysates with or without thrombin receptor-activating peptide (TRAP) stimulation and ii) on platelet concentrates lysates before and after Pathogen inactivation process.
Results: After PI, we observed modulations in the levels of typical markers of autophagy. Indeed, LC3a was increased in platelets when compared to LC3b. ATG5 was also increased suggesting a modulation of autophagy process following PI. The differential levels of ATG5 and LC3a/b were reminiscent of those we observed after TRAP activation of platelet rich plasma. Surprisingly, we could not detect LAMP-2 after TRAP activation, a result that remains to be investigated.
Conclusions: These preliminary results suggest that PI process impacts platelet autophagy which we suggest could contribute to the storage lesions of PC. Despite many connections between autophagy and apoptosis a strong causal relationship wherein one process controls the other, has not been adequately demonstrated in the context of transfusion. Contemporary efforts in elucidating platelet autophagy pathways now allows to focus on the transfusion thematic and help us to understand how autophagy can modulate transfusion yields.
To cite this abstract in AMA style:
Fauteux-Daniel S, Audoux E, Fagan J, Hamzeh-Cognasse H, Eyraud M-, Arthaud C-, Garraud O, Bernard A, Verhoeven P, Laradi S, Cognasse F. Defining the Effects of Storage Lesion on Platelet Autophagic Activity [abstract]. Res Pract Thromb Haemost. 2020; 4 (Suppl 1). https://abstracts.isth.org/abstract/defining-the-effects-of-storage-lesion-on-platelet-autophagic-activity/. Accessed March 21, 2024.« Back to ISTH 2020 Congress
ISTH Congress Abstracts - https://abstracts.isth.org/abstract/defining-the-effects-of-storage-lesion-on-platelet-autophagic-activity/