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CCM2-deficient endothelial cells undergo a ROCK-dependent reprogramming into senescence-associated secretory

Daphné Raphaëlle Vannier1, Apeksha Shapeti2,3, Florent Chuffart1

  • 1Institute for Advanced Biosciences, University Grenoble Alpes, INSERM U1209, CNRS UMR5309, site santé, Allée des Alpes, 38042, Grenoble, France.

Angiogenesis
|August 3, 2021
PubMed
Summary

Defective cerebral cavernous malformation (CCM) cells trigger senescence, invading tissue and attracting other cells. This process is driven by ROCK dysfunction, offering insights into aging and vascular disease.

Keywords:
Cerebral cavernous malformationsMechanotransductionMicroenvironment remodelingROCKSenescence associated secretory phenotype

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Area of Science:

  • Vascular Biology
  • Cellular Aging
  • Mechanobiology

Background:

  • Cerebral cavernous malformation (CCM) involves abnormal brain capillaries.
  • The interplay of mechanotransduction, mosaicism, and inflammation in CCM progression is unclear.

Purpose of the Study:

  • To investigate the role of defective endothelial cells in CCM progression.
  • To elucidate the mechanisms driving CCM pathogenesis, focusing on senescence and cellular interactions.

Main Methods:

  • In vitro silencing of CCM1 and CCM2 genes in endothelial cells.
  • Analysis of senescence-associated secretory phenotype (SASP) induction.
  • Investigation of ROCK pathway involvement in cellular dysfunction and SASP.

Main Results:

  • CCM1- and CCM2-silenced endothelial cells exhibit a senescence-associated secretory phenotype (SASP).
  • SASP promotes extracellular matrix invasion and chemo-attraction of wild-type endothelial and immune cells.
  • ROCK pathway dysfunction drives the observed cytoskeletal, molecular, and transcriptomic disorders, leading to SASP.

Conclusions:

  • CCM2 and ROCK may form a scaffold controlling senescence, linking cell contractility to microenvironment remodeling.
  • SASP in CCM-deficient cells contributes to disease progression by altering the cellular microenvironment.
  • These findings offer novel insights into the control of aging by cellular mechanics in the context of cerebrovascular disease.