Stretch-activated Piezo1 Channel in Endothelial Cells Relaxes Mouse Intrapulmonary Arteries - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue American Journal of Respiratory Cell and Molecular Biology Année : 2019

Stretch-activated Piezo1 Channel in Endothelial Cells Relaxes Mouse Intrapulmonary Arteries

Audrey Lhomme
  • Fonction : Auteur
Thomas Pele
  • Fonction : Auteur
Juliette Deweirdt
  • Fonction : Auteur
Daniel Henrion
  • Fonction : Auteur
Isabelle Baudrimont
  • Fonction : Auteur
Marilyne Campagnac
  • Fonction : Auteur
Roger Marthan
  • Fonction : Auteur
Christelle Guibert
  • Fonction : Auteur
Thomas Ducret
  • Fonction : Auteur
Jean-Pierre Savineau
  • Fonction : Auteur
Jean-François Quignard

Résumé

Abstract After myocardial infarction, resident fibroblasts (Fb) differentiate towards myofibroblasts (MyoFb), generating the scar tissue and the interstitial fibrosis seen in the adjacent myocardium. Fb and MyoFb have the potential to interact with cardiac myocytes (CMs) but insight into the phenotype-specific role and mode of interaction is still incomplete. Our objectives are to further define the modulation of CMs by MyoFbs compared to Fbs, as well as the role of direct contact through gap junctions vs. soluble mediators, using Fbs and CMs from pig left ventricle. Fbs were treated to maintain an undifferentiated state (SD-208) or to attain full differentiation to MyoFb (TGF-β1). Fbs and MyoFbs were co-cultured with CMs, with the possibility of direct contact or separated by a Thincert membrane. Only in direct co-culture, both Fbs and MyoFbs were able to decrease CM viability after 2 days. Only MyoFbs induced significant distal spreading of CMs in both direct and indirect co-culture. MyoFbs, but not Fbs, readily made connections with CMs in direct co-culture and connexin 43 expression in MyoFb was higher than in Fb. When coupled to CMs, MyoFbs reduced the CM action potential duration and hyperpolarized the CM resting membrane potential. Uncoupling reversed these effects. In conclusion, MyoFbs, but not Fbs, alter the CM structural phenotype. MyoFbs, but not Fbs, are likely to electrically connect to CMs and thereby modulate the CM membrane potential. These data provide further support for an active role of MyoFbs in the arrhythmogenic substrate after cardiac remodelling.
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Dates et versions

hal-04491696 , version 1 (06-03-2024)

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Citer

Audrey Lhomme, Guillaume Gilbert, Thomas Pele, Juliette Deweirdt, Daniel Henrion, et al.. Stretch-activated Piezo1 Channel in Endothelial Cells Relaxes Mouse Intrapulmonary Arteries. American Journal of Respiratory Cell and Molecular Biology, 2019, 60 (6), pp.650-658. ⟨10.1165/rcmb.2018-0197oc⟩. ⟨hal-04491696⟩
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