Transcriptome analysis reveals a potential regulatory mechanism of the lnc-5423.6/IGFBP5 axis in the early stages of mouse thymic involution

Acta Biochim Biophys Sin (Shanghai). 2023 Apr 19;55(4):548-560. doi: 10.3724/abbs.2023042.

Abstract

Age-related thymic involution is one of the significant reasons for induced immunity decline. Recent evidence has indicated that lncRNAs are widely involved in regulating organ development. However, the lncRNA expression profiles in mouse thymic involution have not been reported. In this study, we collect mouse thymus at the ages of 1 month, 3 months, and 6 months for sequencing to observe the lncRNA and gene expression profiles in the early stages of thymic involution. Through bioinformatics analysis, a triple regulatory network of lncRNA-miRNA-mRNA that contains 29 lncRNAs, 145 miRNAs and 12 mRNAs that may be related to thymic involution is identified. Among them, IGFBP5 can reduce the viability, inhibit proliferation and promote apoptosis of mouse medullary thymic epithelial cell line 1 (MTEC1) cells through the p53 signaling pathway. In addition, miR-193b-3p can alleviate MTEC1 cell apoptosis by targeting IGFBP5. Notably, lnc-5423.6 can act as a molecular sponge of miR-193b-3p to regulate the expression of IGFBP5. In summary, lnc-5423.6 enhances the expression of IGFBP5 by adsorption of miR-193b-3p, thereby promoting MTEC1 cell apoptosis.

Keywords: IGFBP5; ceRNA; lnc-5423.6; miR-193b-3p; thymic involution.

MeSH terms

  • Animals
  • Gene Expression Profiling
  • Gene Regulatory Networks
  • Mice
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • RNA, Long Noncoding* / genetics
  • RNA, Messenger / genetics
  • Thymus Gland / metabolism
  • Transcriptome

Substances

  • MicroRNAs
  • RNA, Long Noncoding
  • RNA, Messenger
  • IGFBP5-interacting protein, mouse

Grants and funding

This work was supported by the grants from the National Natural Science Foundation of China (No. 31572475), the Guangdong Basic and Applied Basic Research Foundation (No. 2019B1515210011), and the Major Projects of Guangdong Education Department for Foundation Research (No. 2017KZDXM046).