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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Genome-Wide Mapping of Histone Modifications and Transcription Factor Binding Sites in Neuroendocrine Small Cell Lung Cancer Cell Lines Using CUT&RUN
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STING-STAT3-SOX18 Axis Drives EndMT and Epigenetic Reprogramming in SAVI Lung Fibrosis.

Dan Yang1, Guibin Chen1, Sachin Gaurav2

  • 1Translational Vascular Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.

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Summary

Stimulator of interferon genes (STING)-Associated Vasculopathy with onset in infancy (SAVI) patients show high rates of pulmonary fibrosis. STING activation drives endothelial-to-mesenchymal transition, a key process in fibrosis development.

Keywords:
SOX18STAT3STING1endothelial-to-mesenchymal transition (EndMT)fibrosisin-vitro disease model

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Area of Science:

  • Immunology
  • Genetics
  • Pulmonology

Background:

  • A high prevalence of early-onset interstitial lung disease, including pulmonary fibrosis, is observed in pediatric patients with Stimulator of interferon genes (STING)-Associated Vasculopathy with onset in infancy (SAVI).
  • This suggests a critical role for the cGAS-STING pathway in the pathogenesis of pulmonary fibrosis.

Purpose of the Study:

  • To investigate the role of the cGAS-STING pathway in the development of pulmonary fibrosis in SAVI patients.
  • To elucidate the molecular mechanisms underlying STING-mediated endothelial dysfunction and pulmonary fibrosis.

Main Methods:

  • Analysis of lesional lung biopsies from SAVI patients to identify molecular signatures.
  • Generation and characterization of induced pluripotent stem cell-derived endothelial cells (iECs) from SAVI patients with STING1 mutations.
  • Investigation of STING activation effects on endothelial cells, including gene expression and signaling pathways.

Main Results:

  • An endothelial-to-mesenchymal transition (EndMT) signature, characterized by loss of endothelial and gain of mesenchymal markers, was identified in SAVI lung biopsies.
  • SAVI patient-derived iECs with gain-of-function STING1 mutations spontaneously underwent EndMT, which was rescued by isogenic correction.
  • STING activation in endothelial cells induced IRF3-independent STAT3 phosphorylation, initiating a SLUG-dependent mesenchymal program and repressing endothelial maintenance networks.

Conclusions:

  • A non-canonical cGAS-STING-STAT3 signaling axis promotes TGFβ-independent, STING-mediated EndMT and endothelial dysfunction.
  • This pathway contributes to inflammatory pulmonary fibrosis in SAVI.
  • STING represents a potential therapeutic target for inflammatory pulmonary fibrosis.