Volume 4, Issue 4 (Nov 2016)                   Res Mol Med (RMM) 2016, 4(4): 45-50 | Back to browse issues page


XML Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Azhir Z, Hojati Z. Differential Expression of MiR-18b in PBMC from T1D Patients in Isfahan population. Res Mol Med (RMM) 2016; 4 (4) :45-50
URL: http://rmm.mazums.ac.ir/article-1-203-en.html
1- Division of Genetics, Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran.
2- Division of Genetics, Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran. , z.hojati@sci.ui.ac.ir
Abstract:   (5051 Views)

Background: Type 1 diabetes (T1D) is caused by cell-mediated autoimmune attack on pancreatic beta-cells. Previous studies highlight the role of microRNAs (miRNAs) in the pathogenesis of T1D. MiRNAs are small non-coding RNAs involved in the regulation of gene expression post-transcriptionally. In this work, miR-18b was chosen and the differential expression of it was measured between T1D patients and healthy controls from Isfahan population.

Materials and Methods: MiR-18b was selected using Bioinformatics studies by miRWalk software. 22 T1D patients and 18 healthy controls from Isfahan population were enrolled in this study. Total RNA of the peripheral blood mononuclear cells (PBMCs) samples were extracted. After cDNA synthesis, the expression profile of miR-18b quantified by means of qPCR method in patients and controls. Finally the results were statistically analyzed.

Results: In this study despite our hypothesis, the expression levels of miR-18b didn’t show any significant difference between T1D patients and healthy controls (p value: 0.145).

Conclusion: Due to the results of our experimental analysis, it seems that miR-18b doesn’t have any association with T1D disease in Isfahan population.

Full-Text [PDF 540 kb]   (2269 Downloads)    
Type of Study: Research | Subject: Genetic
Published: 2017/03/14

Add your comments about this article : Your username or Email:
CAPTCHA

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

 

Designed & Developed by : Yektaweb