Denatured Albumin Gains a Function of Regulating Platelet Activity

Platelets are blood cells that play a critical role in hemostasis and thrombosis. Serum albumin, which constitutes approximately 50% of plasma proteins, has traditionally been considered non-interactive with platelets and not involved in platelet function. Here, using a molecular force sensor and platelet adhesion and aggregation assays, we show that serum albumin, if denatured, specifically binds to integrins in platelets and transmits platelet contractile forces, regulating platelet activation, adhesion and aggregation as effectively as fibrinogen (the clotting factor I). 0.1% ethanol or 10 micromolar hydrogen peroxide, physiologically attainable in blood through alcohol intake or disease-elevated oxidative stress, are sufficient to denature albumin into a functional platelet ligand. These findings revealed albumin as a previously unrecognized but important regulator of platelet functions, with broad implications for the thrombotic risk in the context of physiological conditions that induce albumin denaturation. ### Competing Interest Statement The authors have declared no competing interest. National Institute of General Medical Sciences, https://ror.org/04q48ey07, R35GM128747 U.S. National Science Foundation, 2204447

Unanchored by two hits: IFNγ and mechanical stress synergize to undermine melanocyte adhesion and promote vitiligo

IFNγ and mechanical stress reduce focal adhesion between melanocytes and the basement membrane. This finding not only advances our understanding of vitilig

Competing forces of polarization and adhesion generate directional migration bias in a minimal model

Left-right axis specification establishes embryonic laterality through asymmetric signaling cascades originating at the cellular scale. We previously reported the presence of a directionality bias in confined pairs of endothelial (and fibroblast) cells exhibiting persistent circular motion, with cytoskeletal contractility modulating the direction. The relative simplicity of the experimental setup makes it a perfect testing ground for the physical forces that could endow this system with a tunable directional migration bias. We model self-propelling biological cells migrating in response to confinement, polarity, and pairwise repulsive forces. Our framework reproduces three key experimental observations: spontaneous coherent circular movement of confined cell pairs, emergence of directional bias when cells have asymmetric properties, and contractility-modulated switching of the rotation direction. Two key assumptions are required: an internal torque arising from cytoskeletal organization (previously observed in other cellular systems), and an asymmetric polarity response between cells, which introduces a difference in how quickly each cell reorients its migration direction. New experiments on daughter cell pairs support this asymmetry requirement in cellular properties. Tuning the polarity response timescale (or strength) relative to centering forces from confinement and cell-cell adhesion can amplify or reverse the directional migration bias.

Spandidos Publications: International Journal of Molecular Medicine

International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

Scaling Laws Governing Droplet Spreading and Merging Dynamics on Solid Surfaces: A Molecular Simulation Study

This study employs molecular dynamics simulations to investigate droplet dynamics when a stationary droplet on a solid surface is struck by another droplet of similar size from above. The focus is on the jumping behavior of the merged droplet and the associated energy conversion. The process is primarily governed by the amount of energy converted into kinetic energy after dissipation. At high impact velocities, the energy conversion efficiency becomes constant, with only about 1% lost due to surface adhesion, an effect that diminishes with increasing velocity. Factors such as impact velocity, droplet size, surface texture, and wettability significantly influence the jumping velocity. Scaling laws are developed for the maximum spreading time, spreading factor, and restitution coefficient based on the Weber (We) and Reynolds (Re) numbers, which differ from those for single droplet impacts. On superhydrophobic surfaces, the spreading time is approximated as three times droplet radius to impact velocity, and its dimensionless form scales linearly with We 0.31. The general scaling laws for the spreading factor for velocity dependent and velocity independent spreading regimes are developed.

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