Integrative microRNA-gene expression network analysis in genetic hypercalciuric stone-forming rat kidney

PeerJ

article

Yuchao Lu¹  Baolong Qin¹  Henglong Hu¹  Jiaqiao Zhang¹  Yufeng Wang¹  Qing Wang¹  Shaogang Wang¹ 

[1] Institute and Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology

关键词: Urolithiasis;    mRNAs;    MicroRNAs;    Microarray;    Idiopathic hypercalciuria;    Genetic hypercalciuric stone-forming rat;   

DOI  :  10.7717/peerj.1884

学科分类：社会科学、人文和艺术（综合）

来源: Inra

【 摘 要 】

Background. MicroRNAs (miRNAs) influence a variety of biological functions by regulating gene expression post-transcriptionally. Aberrant miRNA expression has been associated with many human diseases. Urolithiasis is a common disease, and idiopathic hypercalciuria (IH) is an important risk factor for calcium urolithiasis. However, miRNA expression patterns and their biological functions in urolithiasis remain unknown.Methods and Results. A multi-step approach combining microarray miRNA and mRNA expression profile and bioinformatics analysis was adopted to analyze dysregulated miRNAs and genes in genetic hypercalciuric stone-forming (GHS) rat kidneys, using normal Sprague-Dawley (SD) rats as controls. We identified 2418 mRNAs and 19 miRNAs as significantly differentially expressed, over 700 gene ontology (GO) terms and 83 KEGG pathways that were significantly enriched in GHS rats. In addition, we constructed an miRNA-gene network that suggested that rno-miR-674-5p, rno-miR-672-5p, rno-miR-138-5p and rno-miR-21-3p may play important roles in the regulatory network. Furthermore, signal-net analysis suggested that NF-kappa B likely plays a crucial role in hypercalciuria urolithiasis.Conclusions. This study presents a global view of mRNA and miRNA expression in GHS rat kidneys, and suggests that miRNAs may be important in the regulation of hypercalciuria. The data provide valuable insights for future research, which should aim at validating the role of the genes featured here in the pathophysiology of hypercalciuria.

【 授权许可】

CC BY