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Expression Analysis of Vdr-Related Lncrnas in Autism Spectrum Disorder Publisher Pubmed



Ghafourifard S1 ; Eghtedarian R1 ; Hussen BM2 ; Motevaseli E3 ; Arsangjang S4 ; Taheri M5
Authors
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Authors Affiliations
  1. 1. Department of Medical Genetics, School of Medicine Shahid Beheshti University of Medical Sciences, Tehran, Iran
  2. 2. Department of Pharmacognosy, College of Pharmacy, Hawler Medical University, Erbil, Iraq
  3. 3. Department of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Cancer Gene Therapy Research Center, Zanjan University of Medical Science, Zanjan, Iran
  5. 5. Skull Base Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Source: Journal of Molecular Neuroscience Published:2021


Abstract

Vitamin D receptor (VDR) signaling has been reported to affect neurodevelopment, thus participating in the risk of autism spectrum disorder (ASD). We have measured expression amounts of VDR, CYP27B1, and two related long non-coding RNAs, namely SNHG6 and LINC00511, in the circulation of ASD patients compared with normal controls. Expression of CYP27B1 was remarkably higher in ASD cases compared with controls (posterior beta = 2.38, SE = 0.46, adjusted P value < 0.0001, 95% credible interval (CrI) for beta = [1.49, 3.27]). Level of SNHG6 was lower in ASD cases compared with controls (posterior beta = − 0.791, SE = 0.24, adjusted P value = 0.029, 95% CrI for beta = [− 1.27, − 0.33]). Expression levels of VDR and LINC00511 were similar between ASD cases and controls (P values = 0.97 and 0.46, respectively). Expressions of VDR, CYP27B1, SNHG6, and LINC00511 were not correlated with age of children. However, significant correlations were perceived between expressions of CYP27B1 and LINC00511 (r = 0.47, P < 0.0001), VDR and CYP27B1 (r = 0.42, P < 0.0001), and VDR and SNHG6 (r = 0.32, P < 0.0001). Therefore, these results imply dysregulation of a number of VDR-related genes in ASD patients. © 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.