Plasma membrane and cytoskeleton dynamics during single-cell wound healing

Abstract

Wounding leads not only to plasma membrane disruption, but also to compromised cytoskeleton structures. This results not only in unwarranted exchanges between the cytosol and extracellular milieu, but also in loss of tensegrity, which may further endanger the cell. Tensegrity can be described as the interplay between the tensile forces generated by the apparent membrane tension, actomyosin contraction, and the cytoskeletal structures resisting those changes (e.g., microtubules). It is responsible for the structural integrity of the cell and for its ability to sense mechanical signals. Recent reviews dealing with single-cell healing mostly focused on the molecular machineries controlling the traffic and fusion of specific vesicles, or their role in different pathologies. In this review, we aim to take a broader view of the different modes of single cell repair, while focussing on the different ways the changes in plasmalemma surface area and composition, plasmalemma tension, and cytoskeletal dynamics may influence and affect single-cell repair.

Blood flow restricted training leads to myocellular macrophage infiltration and upregulation of heat shock proteins, but no apparent muscle damage

“…non-chronic) micro-focal alterations in plasma membrane permeability, as previously indicated after acute BFR exercise . Such transient changes in plasma membrane permeability could be a consequence of short duration micro-ruptures in the myofibre membrane (Boucher & Mandato, 2015) or dysfunction in normal membrane transport mechanisms (Gissel, 2005). A transient increase in plasma membrane permeability would allow increased ion influx (e.g.…”

In vitro and ex vivo strategies for intracellular delivery

“…Inundation with reactive oxygen species and other toxic molecules may cause further damage to endogenous proteins and biomolecules 49 . Thus, cells urgently deploy repair pathways to reseal membrane disruptions and recover from the damage imposed (see recent reviews [70][71][72][73][74] ).…”

Cellular mechanisms and signals that coordinate plasma membrane repair

“…This gradient activates different calcium-sensitive responses depending on the local calcium level and the relative affinity of calcium binding proteins [44]. Cells have a variety of calcium sensing proteins that exhibit a wide range of calcium binding affinities, which enables them to mount a diversity of spatially and temporally localized responses to calcium increase (Figure 2) [45]. However, the magnitude and timing for which calcium increase needs to occur for triggering an efficient repair response is variable.…”

“…ATP can be produced by extracellular signals such as calcium and in turn help in propagation of calcium waves for minutes after the initial calcium rise. This may occur by the active release of calcium through plasma membrane calcium ATPases or through signaling by extracellular ligands including ATP [170,45,174]. An abundance of ectoapyrases limits the spatial range of extracellular signaling by ATP.…”