Dysregulated pathways and differentially expressed proteins associated with adverse transfusion reactions in different types of platelet components

Aloui, Chaker; Barlier, Céline; Awounou, Danielle; Thiam, Saliou; Fagan, Jocelyne; Claverol, Stéphane; Tavernier, Emmanuelle; Mounier, Christiane; Hamzeh‐Cognasse, Hind; Cognasse, Fabrice; Garraud, Olivier; Laradi, Sandrine

doi:10.1016/j.jprot.2020.103717

Cited by 4 publications

(4 citation statements)

References 43 publications

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“…A comparison of pooled platelet concentrates and single-donor apheresis platelets-both of which are preparations that occasionally trigger adverse transfusion reactions-revealed a partly common set of proteome changes (i.e., granular and mitochondrial proteins). On the other hand, signalling pathway analysis also revealed some differences: altered integrin α IIb β 3 signalling in the pooled concentrates and acute phase response pathways in the apheresis platelets [46,47].…”

Section: Proteome Changes In Ageing Plateletsmentioning

confidence: 99%

Molecular Proteomics and Signalling of Human Platelets in Health and Disease

Huang

Zhang

Solari

et al. 2021

IJMS

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Platelets are small anucleate blood cells that play vital roles in haemostasis and thrombosis, besides other physiological and pathophysiological processes. These roles are tightly regulated by a complex network of signalling pathways. Mass spectrometry-based proteomic techniques are contributing not only to the identification and quantification of new platelet proteins, but also reveal post-translational modifications of these molecules, such as acetylation, glycosylation and phosphorylation. Moreover, target proteomic analysis of platelets can provide molecular biomarkers for genetic aberrations with established or non-established links to platelet dysfunctions. In this report, we review 67 reports regarding platelet proteomic analysis and signalling on a molecular base. Collectively, these provide detailed insight into the: (i) technical developments and limitations of the assessment of platelet (sub)proteomes; (ii) molecular protein changes upon ageing of platelets; (iii) complexity of platelet signalling pathways and functions in response to collagen, rhodocytin, thrombin, thromboxane A2 and ADP; (iv) proteomic effects of endothelial-derived mediators such as prostacyclin and the anti-platelet drug aspirin; and (v) molecular protein changes in platelets from patients with congenital disorders or cardiovascular disease. However, sample sizes are still low and the roles of differentially expressed proteins are often unknown. Based on the practical and technical possibilities and limitations, we provide a perspective for further improvements of the platelet proteomic field.

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Section: Proteome Changes In Ageing Plateletsmentioning

confidence: 99%

Molecular Proteomics and Signalling of Human Platelets in Health and Disease

Huang

Zhang

Solari

et al. 2021

IJMS

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“…However, lipids are not the main force behind the onset of adverse reactions following platelet transfusion. The processes involved in PC generation (time, temperature) play a role in triggering adverse reactions ( 7 , 25 ). It has been consistently shown that accumulations of Biological Response Modifiers (BRM) are responsible for adverse reactions ( 6 ).…”

Section: Discussionmentioning

confidence: 99%

“…The platelet storage lesion induced platelet activation, decreased the quality of the PC and led to platelet clearance post-transfusion ( 54 ). Proteomic analysis highlights some changes in PC components such as CD40L, PDGF and cytokines (IL1β, IL6, IL27) involved in adverse reaction occurrence ( 7 , 25 , 54 ). Moreover, the state of the patient who received the platelet concentrate transfusion is very important to consider.…”

Section: Discussionmentioning

confidence: 99%

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Bioactive lipids as biomarkers of adverse reactions associated with apheresis platelet concentrate transfusion

et al. 2023

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Platelet concentrate (PC) transfusion seeks to provide haemostasis in patients presenting severe central thrombocytopenia or severe bleeding. PCs may induce adverse reactions (AR) that can occasionally be severe (SAR). PCs contain active biomolecules such as cytokines and lipid mediators. The processing and storage of PCs creates so-called structural and biochemical storage lesions that accumulate when blood products reach their shelf life. We sought to investigate lipid mediators as bioactive molecules of interest during storage and review associations with adverse reactions post-transfusion. To facilitate understanding, we focused on single donor apheresis (SDA) PCs with approximately 31.8% of PCs being delivered in our setting. Indeed, pooled PCs are the most widely transfused products, but the study of a single donor lipid mediator is easier to interpret. We are investigating key lipid mediators involved in AR. Adverse reactions were closely monitored in accordance with current national and regional haemovigilance protocols. Residual PCs were analysed post-transfusion in a series of observations, both with and without severe reactions in recipients. A decrease in the lysophosphatidylcholine species to produce the lysophosphatidic acid species has been observed during storage and in the case of AR. Lysophosphatidic acid increased with primarily platelet-inhibitor lipids. Anti-inflammatory platelet-induced inhibition lipids were weakly expressed in cases of severe adverse reactions. We therefore propose that a decrease in lysophosphatidylcholine and an increase in lysophosphatidic acid can prospectively predict serious adverse transfusion reactions.

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