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Related Experiment Video

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Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model
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Mapping endothelial-cell diversity in cerebral cavernous malformations at single-cell resolution.

Fabrizio Orsenigo1, Lei Liu Conze2, Suvi Jauhiainen2

  • 1Vascular Biology Unit, FIRC Institute of Molecular Oncology Foundation (IFOM), Milan, Italy.

Elife
|November 3, 2020
PubMed
Summary

Cerebral cavernous malformation (CCM) originates from specific venous endothelial cells, not arterial ones. This study reveals cellular origins of CCM lesions using advanced single-cell techniques.

Keywords:
blood brain barriercell biologycerebral cavernous malformationgeneticsgenomicsmousesingle cell RNA sequencingspatial transcriptomicsvascular biologyvascular disease

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Area of Science:

  • Neuroscience
  • Vascular Biology
  • Genetics

Background:

  • Cerebral cavernous malformation (CCM) is a rare neurovascular disorder.
  • CCM is characterized by abnormal blood vessels leading to hemorrhage.
  • Mutations in KRIT1, CCM2, or PDCD10 (CCM3) cause CCM.

Purpose of the Study:

  • To comprehensively characterize brain endothelial cell (EC) subclasses in normal conditions and in a mouse model of CCM.
  • To identify the specific EC subtypes involved in CCM lesion formation.
  • To elucidate the molecular basis of CCM at the single-cell level.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq)
  • Spatial transcriptomics
  • Immunohistochemistry
  • Mouse model of CCM with Pdcd10 deletion

Main Results:

  • Arterial ECs are resistant to CCM transformation.
  • A subset of angiogenic venous capillary ECs and endothelial progenitors are the origin of CCM lesions.
  • scRNA-seq and spatial transcriptomics identified distinct EC subclasses involved in CCM.

Conclusions:

  • CCM development involves specific venous endothelial cell populations.
  • Understanding EC plasticity is key to CCM pathogenesis.
  • This study provides novel single-cell insights into the molecular mechanisms of CCM disease.