Role of MicroRNA-326 and its Target Genes Bcl-xL and Bak as Potential Markers in Platelet Storage Lesion in Blood Banks

Abstract

Platelet transfusion is crucial in the management of various conditions such as quantitative and qualitative platelet disorders. A serious problem that impacts public health is the shortage of Platelet concentrates (PCs) that frequently affect few blood donors’ countries, such as Egypt. This has necessitated the need to establish novel standards for determining the quality of PC during storage. It was found that microRNAs (miRNA) differential expression profile is a helpful tool for recognition of physiological platelet changes during storage. The aim of the current study was to highlight the role of platelet miRNA-326 and its putative target apoptotic genes, Bcl-xL and Bak, and their role in platelet storage lesion (PSL). Differential expression of miRNA-326 and its target genes in the apoptotic pathway, Bcl-xL and Bak was done using quantitative real time PCR (QR-PCR) on different storage points at day 0, day 3 and day 5 in blood bank. The results of the current study revealed over expression of miRNA-326 throughout days of storage resulted in down regulation of Bcl-xL gene and subsequently up regulation of Bak gene. MiRNA-326 contributes to platelet apoptosis and PSL through inhibition of anti-apoptotic Bcl-xL expression and enhancing pro-apoptotic Bak expression. Differential miRNA-326 and its target gene, Bcl-xL and Bak, expression levels at different points of platelets storage are promising tools as biomarkers for platelets undergoing PSL in blood banks.

The platelet storage lesion, what are we working for?

“…microRNA [50][51][52][53][54][55][56][57][58] • miR127 and miR320a increased during 7 days storage and can be biomarkers for platelet function. • miR-326 and miR-145 was positively correlated with platelet function.…”

“… 52 Other miRNAs were associated with platelet apoptosis. Mir‐326 and mir‐let‐7b, which interacted with Bcl‐xL and Bak, had high expression levels during storage, 53 , 54 and mir‐103b downregulating integrin beta 3 (ITGB3) promoted platelet apoptosis. 55 Overexpression of miR‐570‐3p in platelets resulted in reduced levels of mitochondrial ATP synthase subunit g (ATP5L) mRNA and concomitant ATP loss.…”