Profile analysis reveals transfer RNA fragments involved in mesangial cells proliferation

Xiaoyu Lu1, Xianyi Zhu1, Minyi Yu1

  • 1Department of Pediatric Nephrology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210003, China.

Insights

Transfer RNA fragments (tRFs) were investigated as biomarkers for mesangial cell proliferation in glomerulonephritis. Two specific tRFs, tDR-000064 and tDR-000103, were found to be down-regulated and correlated with mesangial cell proliferation.

Area of Science:

  • Molecular Biology
  • Genetics
  • Nephrology

Background:

  • Mesangial cell (MC) proliferation is a key factor in glomerulonephritis pathogenesis.
  • Identifying reliable biomarkers for MC proliferation is crucial for understanding and treating kidney diseases.

Purpose of the Study:

  • To investigate the role of transfer RNA fragments (tRFs) as potential biomarkers for mesangial cell proliferation.
  • To analyze the differential expression of tRFs in proliferating mesangial cells.

Main Methods:

  • Mesangial cells were treated with transforming growth factor-beta 1 (TGF-β1) to induce proliferation.
  • High-throughput sequencing was employed to analyze tRF expression profiles.
  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used for validation.
  • Receiver operating characteristic (ROC) curve analysis was performed to assess diagnostic potential.
  • Gene Ontology (GO) and pathway analysis were conducted.

Main Results:

  • Two tRFs, tDR-000064 and tDR-000103, were significantly down-regulated in TGF-β1-treated (proliferating) mesangial cells compared to normal mesangial cells.
  • tDR-000064 and tDR-000103 expression levels were correlated with mesangial cell proliferation.
  • GO and pathway analysis indicated involvement of these tRFs in MCs and TGF-β1 receptor-mediated signaling.

Conclusions:

  • tDR-000064 and tDR-000103 are potential biomarkers for mesangial cell proliferation.
  • These findings contribute to understanding the molecular mechanisms of glomerulonephritis.
  • Further research into tRFs could offer novel therapeutic targets for kidney diseases.

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