1st International and 10th National Iranian Conference on Bioinformatics
Home Accepted Papers
Investigation of competing endogenous RNA regulation of BCAS4 and SHISA7 in tau pathology in Alzheimer’s disease
Paper ID : 1024-ICB10
Authors:
Hani Sabaie *1, Mohammad Reza Asadi2, Zoha Salkhordeh3, Maryam Rezazadeh2
1Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
2Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
3Department of Medical Genetics, Afzalipour Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran
Abstract:
Alzheimer’s disease (AD) is a heterogeneous neurodegenerative disorder (NDD) that is increasing in prevalence globally [1]. Emerging data suggest that GABAergic signaling may experience pathogenic changes and contribute to the pathological hallmarks of AD, such as tau phosphorylation [2]. Moreover, it is widely established that a disruption in the equilibrium of competing endogenous RNA (ceRNA) crosstalk plays a role in NDDs [3; 4]. In this study, we employed bioinformatic approaches to investigate the ceRNA regulation of BCAS4 and SHISA7 in tau pathology. Two microarray datasets were downloaded from the Gene Expression Omnibus database, including information on mRNAs (GSE106241) and miRNAs (GSE157239) from individuals with AD who had varying degrees of AD-associated neurofibrillary pathology in temporal cortex (TC) tissue specimens and matched controls. The R package limma [5] was used to discover differentially expressed mRNAs and miRNAs associated with AD-related neurofibrillary pathology. We utilized miRWalk (version 3) [6] to identify interactions between miRNAs linked with AD-related neurofibrillary pathology and BCAS4/SHISA7. The ceRNA regulatory axes were constructed utilizing co-expression and miRNA-mRNA interactions. Only Braak stage V exhibited dysregulation of the BCAS4 and SHISA7 genes. Hsa-miR-185-5p targeted both genes BCAS4 and SHISA7 and its levels of expression were statistically higher in TC samples of AD than in controls. Based on co-expression and miRNA-mRNA interactions, BCAS4 was proven to act as a ceRNA for SHISA7 by sponging hsa-miR-185-5p in TC tissue specimens. The current work is the first evidence to highlight the expression of the BCAS4/hsa-miR-185-5p/SHISA7 ceRNA axis in the brains of AD patients.
Keywords:
Alzheimer’s disease; BCAS4; competing endogenous RNA; miR-185; SHISA7
Status : Paper Accepted (Poster Presentation)