Differential microRNA expression in the SH-SY5Y human cell model as potential biomarkers for Huntington’s disease

Journal article

Belkozhayev, Ayaz, Niyazova, Raigul, Kamal, Mohammad Amjad, Ivashchenko, Anatoliy, Sharipov, Kamalidin and Wilson, C. 2024. Differential microRNA expression in the SH-SY5Y human cell model as potential biomarkers for Huntington’s disease. Frontiers in Cellular Neuroscience. 18, p. 1399742. https://doi.org/10.3389/fncel.2024.1399742
AuthorsBelkozhayev, Ayaz, Niyazova, Raigul, Kamal, Mohammad Amjad, Ivashchenko, Anatoliy, Sharipov, Kamalidin and Wilson, C.
AbstractHuntington’s disease (HD) is caused by an expansion of CAG trinucleotide repeat in the HTT gene; the exact pathogenesis of HD currently remains unclear. One of the promising directions in the study of HDs is to determine the molecular mechanism underlying the development and role of microRNAs (miRNAs). This study aimed to identify the profile of miRNAs in an HD human cell line model as diagnostic biomarkers for HD. To study HD, the human SH-SY5Y HD cell model is based on the expression of two different forms: pEGFP-Q23 and pEGFP-Q74 of HTT. The expression of Htt protein was confirmed using aggregation assays combined with immunofluorescence and Western blotting methods. miRNA levels were measured in SH-SY5Y neuronal cell model samples stably expressing Q23 and Q74 using the extraction-free HTG EdgeSeq protocol. A total of 2083 miRNAs were detected, and 354 (top 18 miRNAs) miRNAs were significantly differentially expressed (DE) (p < 0.05) in Q23 and Q74 cell lines. A majority of the miRNAs were downregulated in the HD cell model. Moreover, we revealed that six DE miRNAs target seven genes (ATN1, GEMIN4, EFNA5, CSMD2, CREBBP, ATXN1, and B3GNT) that play important roles in neurodegenerative disorders and showed significant expression differences in mutant Htt (Q74) when compared to wild-type Htt (Q23) using RT-qPCR (p < 0.05 and 0.01). We demonstrated the most important DE miRNA-mRNA profiles, interaction binding sites, and their related pathways in HD using experimental and bioinformatics methods. This will allow the development of novel diagnostic strategies and provide alternative therapeutic routes for treating HD.
KeywordsNucleotide repeats; miRNA; Biomarker; Target genes; Huntington’s disease
Year2024
JournalFrontiers in Cellular Neuroscience
Journal citation18, p. 1399742
PublisherFrontiers Media S.A.
ISSN1662-5102
Digital Object Identifier (DOI)https://doi.org/10.3389/fncel.2024.1399742
Official URLhttps://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2024.1399742/full
Publication dates
Print10 Jul 2024
Online10 Jul 2024
Publication process dates
Accepted26 Jun 2024
Deposited05 Aug 2024
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Open
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