Non-planar Nest-like [Fe2 S2 ] Cluster Sites for Efficient Oxygen Reduction Catalysis.

Metal-nitrogen-carbon catalysts, as promising alternative to platinum-based catalysts for oxygen reduction reaction (ORR), are still highly expected to achieve better performance by modulating the composition and spatial structure of active site. Herein, we constructed the non-planar nest-like [Fe2 S2 ] cluster sites in N-doped carbon plane. Adjacent double Fe atoms effectively weaken the O-O bond by forming a peroxide bridge-like adsorption configuration, and the introduction of S atoms breaks the planar coordination of Fe resulting in greater structural deformation tension, lower spin state, and downward shifted Fe d-band center, which together facilitate the release of OH* intermediate. Hence, the non-planar [Fe2 S2 ] cluster catalyst, with a half-wave potential of 0.92 V, displays superior ORR activity than that of planar [FeN4 ] or [Fe2 N6 ]. This work provides insights into the co-regulation of atomic composition and spatial configuration for efficient oxygen reduction catalysis.

Par3 promotes breast cancer invasion and migration through pull tension and protein nanoparticle-induced osmotic pressure.

Cancer cell invasion and metastasis are closely related to intracellular tension. The cell-polarity protein, Par3, is a mechanical transmitter that affects cytoskeletal forces and determines breast cancer aggressiveness. Increased Par3 tension caused by aPKC inactivation is involved in filopodia and lamellipodia formation. Blocking the connection between Par3 and aPKC increases breast cancer aggressiveness both in vitro and in vivo. Meanwhile, aPKC-induced Par3 cytoplasmic translocation results in JAM-A phase separation and microfilament depolymerization, which is associated with increased intracellular protein nanoparticle-induced osmotic pressure. This study demonstrated the effects of aPKC on Par3 tension and osmotic pressure in breast cancer metastasis, and introduced Par3-associated mechanical mechanisms as potential targets for breast cancer treatment.

Vector Analysis of Cytoskeletal Structural Tension and the Mechanisms that Underpin Spectrin-Related Forces in Pyroptosis.

Aims: Pyroptotic cells are characterized by plasma swelling, membrane blebbing, and disintegration of the cell membrane mediated by spectrin-based membrane skeleton and intercellular competitive tension activities. The spectrin-based membrane skeleton is involved in membrane organization through the regulation of intercellular tension. Using genetically encoded tension sensors to attain noninvasive force measurements in structural proteins, we investigated how cytoskeletal structural tension influences changes in plasma morphology during pyroptosis and the regulatory mechanism of cytoskeletal structural tension that underpins pyroptosis. Results: The results indicate that increasing spectrin tension is caused by osmotic swelling. Hightened tension of spectrin was closely associated with the shrink tension transmitted synergistically by microfilaments (MFs) and microtubules (MTs). However, the increment of spectrin tension in pyroptotic cells was controlled antagonistically by MF and MT forces. Different from MF tension, outward MT forces participated in the formation of membrane blebs. Spectrin tension caused by inward MF forces resisted pyroptosis swelling. Stabilization of MF and MT structure had little influence on intracellular tension and pyroptosis deformation. Pyroptosis-induced cytoskeletal structural tension was highly dependent on calcium signaling and reactive oxygen species generation. Blocking of membrane pores, nonselective ion flux, or elimination of caspase-1 cleavage resulted in the remission of structural forces associated with pyroptosis failure. Innovation and Conclusions: The data suggest that subcellular tension, in terms of magnitude and vector, is integral to pyroptosis through the mediation of swelling and blebbing and the elimination of structural tension, especially MT forces, may result in pyroptosis inhibition.

Analysis of subcellular structural tension in axonal growth of neurons.

The growth and regeneration of axons are the core processes of nervous system development and functional recovery. They are also related to certain physiological and pathological conditions. For decades, it has been the consensus that a new axon is formed by adding new material at the growth cone. However, using the existing technology, we have studied the structural tension of the nerve cell, which led us to hypothesize that some subcellular structural tensions contribute synergistically to axonal growth and regeneration. In this review, we classified the subcellular structural tension, osmotic pressure, microfilament and microtubule-dependent tension involved controllably in promoting axonal growth. A squeezing model was built to analyze the mechanical mechanism underlying axonal elongation, which may provide a new view of axonal growth and inspire further research.