Cortical actin nanodynamics determines nitric oxide release in vascular endothelium

Johannes Fels*, Pia Jeggle, Kristina Kusche-Vihrog, Hans Oberleithner

*Corresponding author for this work
37 Citations (Scopus)


The release of the main vasodilator nitric oxide (NO) by the endothelial NO synthase (eNOS) is a hallmark of endothelial function. We aim at elucidating the underlying mechanism how eNOS activity depends on cortical stiffness (Kcortex) of living endothelial cells. It is hypothesized that cortical actin dynamics determines Kcortex and directly influences eNOS activity. By combined atomic force microscopy and fluorescence imaging we generated mechanical and optical sections of single living cells. This approach allows the discrimination between Kcortex and bulk cell stiffness (Kbulk) and, additionally, the simultaneous analysis of submembranous actin web dynamics. We show that Kcortex softens when cortical F-actin depolymerizes and that this shift from a gel-like stiff cortex to a soft G-actin rich layer, triggers the stiffness-sensitive eNOS activity. The results implicate that stiffness changes in the ~100 nm phase of the submembranous actin web, without affecting Kbulk, regulate NO release and thus determines endothelial function.

Original languageEnglish
Article numbere41520
JournalPLoS ONE
Issue number7
Publication statusPublished - 23.07.2012

Research Areas and Centers

  • Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)


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