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Splicing is the process by which eukaryotic RNA is edited before its translation into protein. The RNA strand transcribed from eukaryotic DNA is called the primary transcript. The primary transcripts that become mRNAs are called precursor messenger RNAs (pre-mRNAs). Eukaryotic pre-mRNA contains alternating sequences of exons and introns. Exons are nucleotide sequences that code for proteins, whereas introns are the non-coding regions. In RNA splicing, introns are removed and exons are bonded...
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Related Experiment Video

Updated: Nov 8, 2025

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
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Splicing factor SRSF6 mediates pleural fibrosis.

Li-Mei Liang1, Liang Xiong1,2, Pei-Pei Cheng3

  • 1Department of Respiratory and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

JCI Insight
|April 27, 2021
PubMed
Summary

The splicing factor SRSF6 is upregulated in pleural fibrosis and drives disease progression by promoting pleural mesothelial cell proliferation and fibrotic protein synthesis. Inhibiting SRSF6 offers a potential therapeutic strategy for treating pleural fibrosis.

Keywords:
FibrosisMouse modelsPulmonology

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Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Molecular Biology

Background:

  • Pleural fibrosis, characterized by excessive extracellular matrix deposition, impairs lung function and is linked to conditions like tuberculous pleurisy.
  • Pleural mesothelial cells (PMCs) are central to fibrosis, but the underlying molecular mechanisms require further elucidation.
  • The role of the RNA-binding splicing factor SRSF6 in pleural fibrosis pathogenesis is currently unknown.

Purpose of the Study:

  • To investigate the role and mechanism of SRSF6 in the development of pleural fibrosis.
  • To determine if SRSF6 levels are altered in patients with tuberculous pleural effusions (TBPE).
  • To evaluate SRSF6 inhibition as a potential therapeutic strategy for pleural fibrosis.

Main Methods:

  • Quantified SRSF6 levels in patient-derived TBPE cells and human PMCs treated with fibrotic stimuli (decellularized TBPE, bleomycin, TGF-β1).
  • Assessed SRSF6's in vitro effects on PMC proliferation and collagen synthesis (COL1A2).
  • Evaluated the in vivo efficacy of SRSF6 inhibition in a mouse model of experimental pleural fibrosis.

Main Results:

  • SRSF6 protein levels were elevated in cells from TBPE and increased in PMCs upon exposure to fibrotic agents.
  • SRSF6 promoted PMC proliferation and COL1A2 synthesis in vitro.
  • SRSF6 inhibition effectively ameliorated experimental pleural fibrosis in mice.
  • SRSF6 upregulation correlated with SMAD2/3 activation, SOX4 increase, and miRNA-506-3p decrease in PMCs.

Conclusions:

  • SRSF6 plays a critical role in inducing pleural fibrosis through pathways involving WNT5A and SMAD1/5/9 signaling.
  • SRSF6 promotes pleural fibrosis by enhancing PMC proliferation and fibrotic matrix production.
  • Targeting SRSF6 presents a promising therapeutic avenue for managing pleural fibrosis.