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MicroRNAs regulating cluster of differentiation 46 (CD46) in cardioembolic and non-cardioembolic stroke
Jun Rong Tan1, Kay Sin Tan2, Fung Lin Yong2
1Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Insights
Cardioembolic stroke, a severe subtype of ischemic stroke, may be diagnosed early using specific microRNAs (miRNAs) that target CD46. These miRNAs show altered levels in patients, aiding in distinguishing stroke types.
Area of Science:
- Biomedical research
- Neurology
- Molecular biology
Background:
- Ischemic stroke poses a significant global health burden, with cardioembolic stroke leading to poor functional outcomes.
- Early diagnosis of cardioembolic stroke is crucial for timely intervention and improved patient prognosis.
- Cluster of differentiation 46 (CD46) is investigated as a potential biomarker for cardioembolic stroke.
Purpose of the Study:
- To investigate microRNAs (miRNAs) that target CD46 as potential diagnostic biomarkers for cardioembolic stroke.
- To analyze the differential expression of CD46 mRNA and specific miRNAs in various ischemic stroke subtypes.
- To assess the diagnostic accuracy of these miRNAs in differentiating cardioembolic from non-cardioembolic stroke.
Main Methods:
- Bioinformatic analysis to identify miRNAs targeting CD46 mRNA.
- Luciferase reporter assays to confirm miRNA-CD46 interactions.
- Quantitative analysis of CD46 mRNA and miRNA levels in patient samples from different stroke subtypes.
- Receiver Operating Characteristic (ROC) curve analysis to evaluate diagnostic performance.
Main Results:
- CD46 mRNA levels were significantly different between cardioembolic and non-cardioembolic stroke subtypes.
- miR-19a, miR-20a, miR-185, and miR-374b were identified as CD46-targeting miRNAs.
- Levels of these miRNAs were significantly reduced in non-cardioembolic stroke patients compared to cardioembolic stroke patients.
- miRNAs demonstrated higher diagnostic accuracy (AUC) than CD46 in distinguishing cardioembolic stroke.
- miR-19a and miR-20a were found to regulate CD46 expression in Human Umbilical Vein Endothelial Cells (HUVECs).
Conclusions:
- Specific miRNAs targeting CD46, particularly miR-19a and miR-20a, show potential as sensitive biomarkers for early cardioembolic stroke diagnosis.
- These miRNAs may play a role in the pathogenesis of cardioembolic stroke, potentially through endothelial cell mechanisms.
- Further research into these miRNA-CD46 interactions could lead to novel diagnostic and therapeutic strategies for cardioembolic stroke.
Abstract:
Ischemic stroke is a major cause of mortality and morbidity globally. Among the ischemic stroke subtypes, cardioembolic stroke is with poor functional outcome (Modified Rankin score ≥ 2). Early diagnosis of cardioembolic stroke will prove beneficial. This study examined the microRNAs targeting cluster of differentiation 46 (CD46), a potential biomarker for cardioembolic stroke. CD46 mRNA level was shown to be differentially expressed (p < 0.001) between cardioembolic stroke (median = 1.32) and non-cardioembolic stroke subtypes (large artery stroke median = 5.05; small vessel stroke median = 6.45). Bioinformatic search showed that miR-19a, -20a, -185 and -374b were found to target CD46 mRNA and further verified by luciferase reporter assay. The levels of miRNAs targeting CD46 were significantly reduced (p < 0.05) in non-cardioembolic stroke patients (large artery stroke median: miR-19a = 0.63, miR-20a = 0.42, miR-185 = 0.32, miR-374b = 0.27; small artery stroke median: miR-19a = 0.07, miR-20a = 0.06, miR-185 = 0.07, miR-374b = 0.05) as compared to cardioembolic stroke patients (median: miR-19a = 2.69, miR-20a = 1.36, miR-185 = 1.05, miR-374b = 1.23). ROC curve showed that the miRNAs could distinguish cardioembolic stroke from non-cardioembolic stroke with better AUC value as compared to CD46. Endogenous expression of CD46 in Human Umbilical Vein Endothelial Cells (HUVECs) were found to be regulated by miR-19a and miR-20a. Thus implicating that miR-19a and -20a may play a role in pathogenesis of cardioembolic stroke, possibly via the endothelial cells.
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