Open Access

Expression profiles of tRNA‑derived fragments in high glucose‑treated tubular epithelial cells

  • Authors:
    • Jialing Ji
    • Ju Rong
    • Hui Zheng
    • Huimin Shi
    • Gaoting Qu
    • Shanwen Li
    • Weihua Gan
    • Aiqing Zhang
  • View Affiliations

  • Published online on: November 23, 2022     https://doi.org/10.3892/etm.2022.11725
  • Article Number: 26
  • Copyright: © Ji et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Transfer RNA‑derived fragments (tRFs), a novel class of small non‑coding RNA produced by the cleavage of pre‑ and mature tRNAs, are involved in various diseases. Renal tubulointerstitial fibrosis is a common final pathway in diabetic nephropathy (DN) in which hyperglycemia‑induced tubular extracellular matrix (ECM) accumulation serves a vital role. The present study aimed to detect and investigate the role of tRFs in the accumulation of tubular ECM. Differentially expressed tRFs were analysed with high‑throughput sequencing in primary mouse tubular epithelial cells treated with high glucose (HG). The Gene Ontology (GO) was used to analyze the potential molecular functions of these differentially expressed tRFs, and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to analyze the associated signaling pathways involved in these differentially expressed tRFs. tRF‑1:30‑Gln‑CTG‑4 was overexpressed using tRF‑1:30‑Gln‑CTG‑4 mimic, followed by HG treatment. A total of 554 distinct tRFs were detected and 64 differentially expressed tRFs (fold change >2; P<0.05) were identified in tubular epithelial cells following high glucose (HG) treatment, among which 27 were upregulated and 37 were downregulated. Ten selected tRFs with the greatest difference (fold change >2; P<0.05) were verified to be consistent with small RNA‑sequencing data, of which tRF‑1:30‑Gln‑CTG‑4 showed the most pronounced difference in expression and was significantly decreased in response to HG. GO analysis indicated that the differentially expressed tRFs were associated with ‘cellular process’, ‘biological regulation’ and ‘metabolic process’. An analysis of the KEGG database suggested that these differentially expressed tRFs were involved in ‘autophagy’ and signaling pathways for ‘forkhead box O’, ‘the mammalian target of rapamycin’ and ‘mitogen‑activated protein kinase’. Finally, the overexpression of tRF‑1:30‑Gln‑CTG‑4 ameliorated HG‑induced ECM accumulation in tubular epithelial cells. Therefore, the present study demonstrated that there may be a significant association between tRFs and HG‑induced ECM accumulation in tubular epithelial cells; these differentially expressed tRFs warrant further study to explore the pathogenesis of DN.
View Figures
View References

Related Articles

Journal Cover

January-2023
Volume 25 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Ji J, Rong J, Zheng H, Shi H, Qu G, Li S, Gan W and Zhang A: Expression profiles of tRNA‑derived fragments in high glucose‑treated tubular epithelial cells. Exp Ther Med 25: 26, 2023
APA
Ji, J., Rong, J., Zheng, H., Shi, H., Qu, G., Li, S. ... Zhang, A. (2023). Expression profiles of tRNA‑derived fragments in high glucose‑treated tubular epithelial cells. Experimental and Therapeutic Medicine, 25, 26. https://doi.org/10.3892/etm.2022.11725
MLA
Ji, J., Rong, J., Zheng, H., Shi, H., Qu, G., Li, S., Gan, W., Zhang, A."Expression profiles of tRNA‑derived fragments in high glucose‑treated tubular epithelial cells". Experimental and Therapeutic Medicine 25.1 (2023): 26.
Chicago
Ji, J., Rong, J., Zheng, H., Shi, H., Qu, G., Li, S., Gan, W., Zhang, A."Expression profiles of tRNA‑derived fragments in high glucose‑treated tubular epithelial cells". Experimental and Therapeutic Medicine 25, no. 1 (2023): 26. https://doi.org/10.3892/etm.2022.11725