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Transcriptomic analysis implicates the involvement of RBM20 in Fuchs' endothelial corneal dystrophy with TCF4 repeat

Xunzhi Zhang1, Ze Yu1, Aundrea K Westfall1,2

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This summary is machine-generated.

Ribonucleic acid binding motif protein 20 (RBM20) may drive Fuchs

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Area of Science:

  • Ophthalmology
  • Genetics
  • Molecular Biology

Background:

  • Late-onset Fuchs' endothelial corneal dystrophy (FECD) is a corneal degenerative disease.
  • A trinucleotide repeat expansion (CTG18.1) in the TCF4 gene causes two-thirds of FECD cases.
  • Transcriptomic profiles of FECD with (RE+) and without (RE-) the expansion show high similarity, obscuring molecular mechanisms.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying FECD.
  • To differentiate between FECD with repeat expansion (RE+) and without (RE-).

Main Methods:

  • Analysis of publicly available RNA sequencing datasets from human corneal endothelial tissues.
  • Comparison of gene expression profiles between RE+ and RE- transcriptomic data.
  • Utilized upstream regulator analysis, alternative splicing analysis, and motif enrichment analysis.

Main Results:

  • Upregulated expression of ribonucleic acid binding motif protein 20 (RBM20) observed in both RE+ cases and controls.
  • RBM20 motif enrichment in skipped exon events in RE+ subjects compared to RE- subjects.
  • Skipped exon events in DST, FNBP1, and SORBS1 were consistently identified in RE+ subjects.

Conclusions:

  • RBM20 may be an RE+-specific factor in FECD pathogenesis.
  • Increased RBM20 expression in RE+ individuals could contribute to FECD by repressing exon inclusion.