Significant reductions in apoptosis-related proteins (HSPA6, HSPA8, ITGB3, YWHAH, and PRDX6) are involved in immune thro
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Significant reductions in apoptosis‑related proteins (HSPA6, HSPA8, ITGB3, YWHAH, and PRDX6) are involved in immune thrombocytopenia Shu‑yan Liu1 · Dai Yuan1,2 · Rui‑Jie Sun1 · Jing‑jing Zhu2 · Ning‑ning Shan1,2 Accepted: 5 October 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract To investigate differences in the expression of plasma proteins in immune thrombocytopenia (ITP) and normal control groups, bone marrow samples were collected from 20 active ITP patients and 20 healthy controls. Quantitative proteomics analysis based on mass spectrometry was used to measure the protein levels and understand the protein networks. We found differentially expressed proteins in ITP patients and healthy controls. Parallel reaction monitoring (PRM), a targeted proteome quantification technique, was used to quantitatively confirm the identified target proteins and verify the proteomics data. In this study, a total of 829 proteins were identified, and the fold-change cut-off was set at 1.5 (patients vs controls); a total of 26 proteins were upregulated, and 69 proteins were downregulated. The bioinformatics analysis indicated that some differentially expressed proteins were associated with apoptosis. KEGG enrichment analysis showed that the apoptosis-related proteins were closely related to the PI3K-Akt signalling pathway. PRM demonstrated that apoptosis-related proteins were significantly decreased in ITP patients, which further confirmed the important effect of apoptosis on ITP pathogenesis. We hypothesised that apoptosis may be closely related to ITP pathogenesis through the PI3K-Akt signalling pathway. Keywords Immune thrombocytopenia · Apoptosis · PI3K-akt signalling pathway
Highlights • Apoptosis-related proteins (HSPA6, HSPA8, ITGB3,
YWHAH, and PRDX6) were differentially downregulated in ITP. • Apoptosis may be closely related to ITP pathogenesis through the PI3K-Akt signalling pathway.
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11239-020-02310-5) contains supplementary material, which is available to authorized users. * Ning‑ning Shan [email protected] 1
Department of Hematology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250021, Shandong, China
Department of Hematology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, 324 Jing Wu Rd, Jinan 250021, Shandong, China
2
Introduction Immune thrombocytopenia (ITP) is an autoimmune-mediated bleeding disorder characterized by a low platelet count, and the clinical symptoms are a reduction in platelets in the peripheral blood, mucocutaneous haemorrhage, and visceral haemorrhage [1]. The underlying mechanism involves the production of platelet membrane antigen-specific IgG autoantibodies, such as glycoprotein (GP) IIb/IIIa and GPIB/ IX, and these anti-platelet autoantibodies attack megakaryocytes expressing GPIIb/IIIa and GPIb/IX. Recent studies on the pathogenesis of ITP have focused on apoptosis, which may le
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