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Haemodynamic and extracellular matrix cues regulate the mechanical phenotype and stiffness of aortic endothelial cells

Author

Listed:
  • Caitlin Collins

    (University of North Carolina at Chapel Hill)

  • Lukas D. Osborne

    (University of North Carolina at Chapel Hill)

  • Christophe Guilluy

    (University of North Carolina at Chapel Hill)

  • Zhongming Chen

    (University of North Carolina at Chapel Hill)

  • E. Tim O’Brien

    (University of North Carolina at Chapel Hill)

  • John S. Reader

    (University of North Carolina at Chapel Hill)

  • Keith Burridge

    (University of North Carolina at Chapel Hill
    Lineberger Cancer Center, University of North Carolina at Chapel Hill
    McAllister Heart Institute, University of North Carolina at Chapel Hill)

  • Richard Superfine

    (University of North Carolina at Chapel Hill)

  • Ellie Tzima

    (University of North Carolina at Chapel Hill
    Lineberger Cancer Center, University of North Carolina at Chapel Hill
    McAllister Heart Institute, University of North Carolina at Chapel Hill)

Abstract

Endothelial cells (ECs) lining blood vessels express many mechanosensors, including platelet endothelial cell adhesion molecule-1 (PECAM-1), that convert mechanical force into biochemical signals. While it is accepted that mechanical stresses and the mechanical properties of ECs regulate vessel health, the relationship between force and biological response remains elusive. Here we show that ECs integrate mechanical forces and extracellular matrix (ECM) cues to modulate their own mechanical properties. We demonstrate that the ECM influences EC response to tension on PECAM-1. ECs adherent on collagen display divergent stiffening and focal adhesion growth compared with ECs on fibronectin. This is because of protein kinase A (PKA)-dependent serine phosphorylation and inactivation of RhoA. PKA signalling regulates focal adhesion dynamics and EC compliance in response to shear stress in vitro and in vivo. Our study identifies an ECM-specific, mechanosensitive signalling pathway that regulates EC compliance and may serve as an atheroprotective mechanism that maintains blood vessel integrity in vivo.

Suggested Citation

  • Caitlin Collins & Lukas D. Osborne & Christophe Guilluy & Zhongming Chen & E. Tim O’Brien & John S. Reader & Keith Burridge & Richard Superfine & Ellie Tzima, 2014. "Haemodynamic and extracellular matrix cues regulate the mechanical phenotype and stiffness of aortic endothelial cells," Nature Communications, Nature, vol. 5(1), pages 1-12, September.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4984
    DOI: 10.1038/ncomms4984
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    Cited by:

    1. Lanlan Zhang & Xuezhen Gui & Ruijie Hou & Liping Jia & Shu Xia & Xin Zhang & Yingyun Fu & Qian-Fang Meng & Qun Luo & Xing Shi & Bingxin Guo & Ruifang Liang & Ludan Yue & Xue Chen & Haizhao Xu & Pengbo, 2026. "Single-cell multiomics uncovers an endothelial mechanosensitive PIEZO1-IL-33 axis driving pulmonary fibrosis," Nature Communications, Nature, vol. 17(1), pages 1-17, December.

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