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Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption

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Quantifying intracellular mechanosensitive response upon spatially defined mechano-chemical triggering.

Elaheh Zare-Eelanjegh¹, Renard T M Lewis², Ines Lüchtefeld¹

¹Laboratory of Biosensors and Bioelectronics, Institute for Biomedical Engineering, ETH Zurich, Zurich, Switzerland.

|June 17, 2026

Summary

Cellular force transmission involves mechanical and biochemical signals. This study reveals distinct roles for A- and B-type lamins in nuclear mechanotransduction and how microtubules adapt to tension, offering insights for treating mechanical stress diseases.

Keywords:

HeLa cells cytoskeleton endoplasmic reticulum mechanoresponse lamins mechanotransmission nuclear mechanoresponse physics of living systems

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Area of Science:

Cell Biology
Biophysics
Mechanobiology

Background:

Mechanotransduction converts mechanical stimuli into biochemical signals via cellular components like actin, microtubules, and the nuclear lamina.
Understanding the nuclear lamina's role in mechanotransmission is crucial for cellular force response.
Fluidic Force Microscopy (FluidFM) offers a method for in situ mechanical and chemical cell manipulation.

Purpose of the Study:

To investigate the distinct roles of A- and B-type lamins in the nuclear mechanotransduction process.
To explore how nuclear lamina composition influences cellular responses to external mechanical cues.
To elucidate the dynamic behavior of microtubules in response to altered nuclear lamina states.

Main Methods:

Utilized Fluidic Force Microscopy (FluidFM) for mechanical manipulation of cells.
Employed Fluorescence Lifetime Imaging Microscopy (FLIM) for high-resolution mapping of intracellular tension.
Examined cells with varying nuclear lamina compositions, including lamin A/C knockout models.

Main Results:

A-type lamins were found to contribute to nuclear elasticity, while B-type lamins influenced viscous response.
Microtubules exhibited mechanical adaptation, releasing tension in lamin A/C knockout cells.
In healthy cells, microtubules preserved local tension, unlike in knockout cells where they aided tension release.

Conclusions:

Nuclear lamins (A- and B-type) play distinct roles in initiating and modulating nuclear mechanotransduction.
Microtubule dynamics are crucial for adapting to and regulating cellular tension, particularly in the absence of specific lamins.
Findings provide insights into cellular mechanosensing and potential therapeutic targets for diseases linked to mechanical stress.