Identification of novel biomarkers in chronic immune thrombocytopenia (ITP) by microarray-based serum protein profiling. | - CCMAR -

Journal Article

TítuloIdentification of novel biomarkers in chronic immune thrombocytopenia (ITP) by microarray-based serum protein profiling.
Publication TypeJournal Article
AuthorsBal, G, Futschik, ME, Hartl, D, Ringel, F, Kamhieh-Milz, J, Sterzer, V, Hoheisel, JD, Alhamdani, MSS, Salama, A
Year of Publication2016
JournalBr J Haematol
Date Published2016 Feb
Palavras-chaveAutoantibodies, Biomarkers, Blood Platelets, Case-Control Studies, Chronic Disease, Core Binding Factor Alpha 2 Subunit, Core Binding Factor Alpha 3 Subunit, Enzyme-Linked Immunosorbent Assay, Humans, Neoplasm Proteins, Proliferating Cell Nuclear Antigen, Protein Array Analysis, Purpura, Thrombocytopenic, Idiopathic, Reverse Transcriptase Polymerase Chain Reaction, RNA, Messenger, Vascular Endothelial Growth Factor A

The pathological mechanisms underlying the development of immune thrombocytopenia (ITP) are unclear and its diagnosis remains a process of exclusion. Currently, there are no known specific biomarkers for ITP to support differential diagnosis and treatment decisions. Profiling of serum proteins may be valuable for identifying such biomarkers. Sera from 46 patients with primary chronic ITP and 34 healthy blood donors were analysed using a microarray of 755 antibodies. We identified 161 differentially expressed proteins. In addition to oncoproteins and tumour-suppressor proteins, including apoptosis regulator BCL2, breast cancer type 1 susceptibility protein (BRCA1), Fanconi anaemia complementation group C (FANCC) and vascular endothelial growth factor A (VEGFA), we detected six anti-nuclear autoantibodies in a subset of ITP patients: anti-PCNA, anti-SmD, anti-Ro/SSA60, anti-Ro/SSA52, anti-La/SSB and anti-RNPC antibodies. This finding may provide a rational explanation for the association of ITP with malignancies and other autoimmune diseases. While RUNX1mRNA expression in the peripheral blood mononuclear cells (PBMC) of patients was significantly downregulated, an accumulation of RUNX1 protein was observed in the platelets of ITP patients. This may indicate dysregulation of RUNX1 expression in PBMC and megakaryocytes and may lead to an imbalanced immune response and impaired thrombopoiesis. In conclusion, we provide novel insights into the pathogenic mechanisms of ITP that warrant further exploration.


Alternate JournalBr. J. Haematol.
PubMed ID26628061
CCMAR Authors