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Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model

Published on: September 4, 2017

Sulindac metabolites decrease cerebrovascular malformations in CCM3-knockout mice.

Luca Bravi¹, Noemi Rudini¹, Roberto Cuttano¹

¹Fondazione Italiana per la Ricerca sul Cancro (FIRC) Institute of Molecular Oncology Fondazione, 20139 Milan, Italy;

Proceedings of the National Academy of Sciences of the United States of America

|June 26, 2015

Summary

This summary is machine-generated.

Researchers found that anti-inflammatory drugs sulindac sulfide and sulindac sulfone can reduce vascular malformations in cerebral cavernous malformation (CCM) disease, offering new hope for pharmacological therapy.

Keywords:

cerebral cavernous malformation endothelial cells sulindac metabolites vascular pathology β-catenin

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Published on: January 27, 2015

Area of Science:

Neuroscience
Vascular Biology
Pharmacology

Background:

Cerebral cavernous malformation (CCM) is a neurological disease characterized by hemorrhage-prone vascular malformations.
Current treatment for CCM is primarily surgical, which is often not feasible.
There is a significant need for effective pharmacological treatments for CCM.

Purpose of the Study:

To investigate the molecular mechanisms underlying CCM development.
To identify potential therapeutic targets for CCM.
To evaluate the efficacy of specific anti-inflammatory drugs in reducing CCM-related vascular malformations.

Main Methods:

Development of a murine model of CCM through endothelial-cell-specific ablation of the CCM3 gene.
Analysis of β-catenin transcription activity in CCM3-deficient endothelial cells in vitro and in vivo.
Assessment of the impact of sulindac sulfide and sulindac sulfone on vascular malformations in the CCM mouse model.

Main Results:

CCM3 deficiency in endothelial cells leads to early, cell-autonomous Wnt-receptor-independent stimulation of β-catenin transcription.
A β-catenin-driven transcription program triggers endothelial-to-mesenchymal transition, with TGF-β/BMP signaling required for disease progression.
Administration of sulindac sulfide and sulindac sulfone attenuated β-catenin transcription activity and reduced vascular malformations in CCM3-deficient mice.

Conclusions:

CCM pathogenesis involves early β-catenin activation and endothelial-to-mesenchymal transition.
Sulindac sulfide and sulindac sulfone demonstrate therapeutic potential for CCM by targeting β-catenin signaling.
This research opens new avenues for pharmacological treatment of intracranial vascular cavernomas.