Identification of transfer RNA-derived fragments and their potential roles in aortic dissection

Xiuxiu Fu, Xingqiang He, Yanyan Yang, Shaoyan Jiang, Shizhong Wang, Xingang Peng, Guozhang Tang, Tingyu Zong, Xiaolu Li, Ying Zhang, Yulin Zou, Tao Yu

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)

Abstract

Emerging evidence suggests that majority of the transfer RNA (tRNA)-derived small RNA, including tRNA-derived fragments (tRFs) and tRNA halves (tiRNAs), play a significant role in the molecular mechanisms underlying some human diseases. However, expression of tRFs/tiRNAs and their potential roles in aortic dissection (AD) remain unclear. This study examined the expression characteristics and explored the functional roles of tRFs/tiRNAs in AD using RNA-sequencing, bioinformatics, real-time quantitative reverse transcription polymerase chain reaction, and loss- and gain-of-function analysis. Results revealed that a total of 41 tRFs/tiRNAs were dysregulated in the AD group compared to the control group. Among them, 12 were upregulated and 29 were downregulated (fold change≥1.5 and p < 0.05). RT-qPCR results revealed that expressions of tRF-1:30-chrM.Met-CAT was significantly upregulated, while that of tRF-54:71-chrM.Trp-TCA and tRF-1:32-chrM.Cys-GCA were notably downregulated; expression patterns were consistent with the RNA sequencing data. Bioinformatic analysis showed that a variety of related pathways might be involved in the pathogenesis of AD. Functionally, tRF-1:30-chrM.Met-CAT could facilitate proliferation, migration, and phenotype switching in vascular smooth muscle cells (VSMCs), which might serve as a significant regulator in the progression of AD. In summary, the study illustrated that tRFs/tiRNAs expressed in AD tissues have potential biological functions and may act as promising biomarkers or therapeutic targets for AD.

Original languageEnglish
Pages (from-to)3039-3049
Number of pages11
JournalGenomics
Volume113
Issue number5
DOIs
Publication statusPublished - Sept 2021
Externally publishedYes

Bibliographical note

Funding Information:
This work was supported by The National Natural Science Foundation of China (grant no. 81870331), The Qingdao municipal science and technology bureau project (grant no. 21–1-4-rkjk-12-nsh), and Qingdao University Medical Group Project (YLJT20201012).

Publisher Copyright:
© 2021 Elsevier Inc.

ASJC Scopus Subject Areas

  • Genetics

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't

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