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Epigenetic regulation by polycomb repressive complex 1 promotes cerebral cavernous malformations.

Van-Cuong Pham1, Claudia Jasmin Rödel1, Mariaelena Valentino2

  • 1Institute of Biochemistry and Biology, Potsdam University, D-14476, Potsdam, Germany.

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|October 14, 2024
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Chromobox Protein Homolog 7 (CBX7) drives pathological signaling in cerebral cavernous malformations (CCMs). Inhibiting CBX7 reduces CCMs in preclinical models, offering new therapeutic avenues for this vascular disorder.

Keywords:
CBX7Cerebral Cavernous MalformationKLF2WNT9endoMT

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Area of Science:

  • Vascular Biology
  • Genetics
  • Molecular Biology

Background:

  • Cerebral cavernous malformations (CCMs) are vascular anomalies.
  • Loss of CCM proteins initiates a MAPK-Krüppel-like factor 2 (KLF2) signaling cascade.
  • Downstream KLF2 target genes in CCM pathogenesis are largely unidentified.

Purpose of the Study:

  • To investigate the role of Chromobox Protein Homolog 7 (CBX7) in KLF2-mediated signaling in CCMs.
  • To determine if CBX7 inhibition can ameliorate CCM phenotypes.

Main Methods:

  • Analysis of CBX7/cbx7a mRNA expression in CCM patient lesions and CCM-deficient cells (human, mouse, zebrafish).
  • Silencing or pharmacological inhibition of CBX7/Cbx7a in zebrafish, HUVECs, and a murine CCM3 model.
  • Whole-transcriptome analysis to identify KLF2 target genes regulated by CBX7.

Main Results:

  • CBX7 is upregulated in CCM lesions and CCM-deficient endothelial cells.
  • CBX7 inhibition significantly suppresses pathological CCM phenotypes across multiple models.
  • CBX7 regulates KLF2 target genes, including TEK, ANGPT1, WNT9, and genes associated with endothelial-mesenchymal transition (endoMT).

Conclusions:

  • CBX7 is a key regulator of KLF2-dependent biomechanical signaling in CCM pathogenesis.
  • Targeting CBX7 presents a promising therapeutic strategy for cerebral cavernous malformations.