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

Genomics

Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, Qingdao 266000, China; Institute for Translational Medicine, The Affiliated Hospital of Qingdao University, No. 38 Dengzhou Road, Qingdao 266021, People's Republic of China.. Electronic address:

Published: September 2021

AI Article Synopsis

  • A recent study found that tRNA-derived small RNAs (tRFs and tiRNAs) are involved in the mechanisms of aortic dissection (AD), though their roles remain unclear.
  • The research identified 41 dysregulated tRFs/tiRNAs in AD patients, with 12 being upregulated and 29 downregulated, and confirmed these findings with real-time quantitative PCR.
  • One specific tRF, tRF-1:30-chrM.Met-CAT, was linked to promoting cell growth and movement in vascular smooth muscle cells, suggesting these tRNAs could be useful as biomarkers or targets for AD treatment.

Article 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.

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http://dx.doi.org/10.1016/j.ygeno.2021.06.039DOI Listing

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