학술논문

Aberrant Expression of miRNA and mRNAs in Lesioned Tissues of Graves' Disease.
Document Type
Article
Source
Cellular Physiology & Biochemistry (Karger AG). Apr2015, Vol. 35 Issue 5, p1934-1942. 9p.
Subject
*MICRORNA
*AUTOIMMUNE diseases
*GRAVES' disease
*GENE expression
*GENETIC regulation
Language
ISSN
1015-8987
Abstract
Background and Aims: Abnormal microRNA (miRNA) expression is found in many diseases including autoimmune diseases. However, little is known about the role of miRNA regulation in Graves' disease (GD). Here, we simultaneously detected different expressions of miRNA and mRNAs in thyroid tissues via a high-throughput transcriptomics approach, known as microarray, in order to reveal the relationship between aberrant expression of miRNAs and mRNAs spectrum and GD. Methods: Totally 7 specimens of thyroid tissue from 4 GD patients and 3 controls were obtained by surgery for microarray analysis. Then, 30 thyroid specimens (18 GD and 12 controls) were also collected for further validation by quantitative real-time PCR ( qRT-PCR ). Results: Statistical analysis showed that the expressions of 5 specific miRNA were increased significantly while those of other 18 miRNA were decreased in thyroid tissue of GD patients (FC≥1.3 or≤0.77 and p<0.05). In addition, the transcription of 1271 mRNAs was up-regulated, while the expression of 777 mRNAs transcripts was down-regulated (FC≥2.0 or≤0.5 and p<0.05). Furthermore, integrated analysis of differentially expressed miRNA and their target mRNAs demonstrated that 2 miRNA (miR-22 and miR-183) were increased while their potential target mRNAs were decreased. 3 miRNA (miR-101, miR-197 and miR-660) were decreased while their potential target mRNAs were increased. The above findings from microarray screening were confirmed by qRT-PCR in more samples. The results were consistent with those observed in the microarray assays. Conclusion: Our study highlights the possibility that miRNA-target gene network may be involved in the pathogenesis of GD and could provide new insights into understanding the pathophysiological mechanisms of GD. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]