Microfluidics and low-Reynolds flow
Does the kind of flow force change how cells deform?
Open access · cc by · source: Europe PMC
Cells squeezed in a microchannel look stiffer under inertial forces than under viscous shear of the same size, so the type of force decides which parts of the cell you are probing.
Study at a glance
- Design
- Other — High-speed imaging of cells deformed at the stagnation point of a cross-flow microfluidic junction across flow rates and suspension viscosities (1 to 33 cP), with Kelvin-Voigt model fits
- N
- No overall cell count reported; the averaged strain trace used 50 HL60 cells, and many deformation events were imaged per flow condition.
- Population
- HL60 leukaemia cells, SW480 colorectal cancer cells, and SW480 cells treated with the actin disruptor latrunculin A
- Outcome
- Deformation index, strain versus time, deformation and relaxation times, elastic modulus, post-deformation viability
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Key findings
In the inertial regime the deformation index plateaued near 1.70 up to about 400 microlitres per minute (a yield point where actin breaks down), rose further, and cells ruptured beyond about 600, where viability fell below 50%. For the same force, cells deformed more in the shear regime, and the maximum deformation rose linearly with viscosity. The shear regime at low flow best detected actin disruption, while differences between the two cell lines grew at high flow. The fitted elastic modulus of HL60 cells was 0.30 kPa, and relaxation time separated all three cell groups, with HL60 relaxing about 2.5 times more slowly than SW480.
Methodology
The authors pushed single cells into a cross-shaped channel where two opposing flows meet and filmed them at up to 260,000 frames per second as they stretched at the stagnation point. By changing flow rate and adding methylcellulose to raise viscosity from 1 to 33 cP, they switched between an inertia-dominated and a shear-dominated regime in one device. They compared soft circulating leukaemia cells, stiffer colorectal tumour cells, and tumour cells whose actin was disrupted by latrunculin A, and fitted a spring-and-dashpot (Kelvin-Voigt) model to strain-versus-time traces.
Limitations
Only two cell lines and one drug were tested, so the claims about which regime probes the cytoskeleton versus the nucleus are suggestive rather than established; the nuclear explanation is a hypothesis based on nuclear size ratios. The Kelvin-Voigt model is a simple approximation and the stress profile was assumed to be sinusoidal. High viscosity limited the flow rates reachable, and moduli from different techniques disagree, so absolute values depend on method.
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