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 language | English |
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Pages (from-to) | 3039-3049 |
Number of pages | 11 |
Journal | Genomics |
Volume | 113 |
Issue number | 5 |
DOIs | |
Publication status | Published - Sept 2021 |
Externally published | Yes |
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