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Figure 2). Mechanical lesions lead to high, localized levels of membrane integrity loss, tension
change and Ca2+ inux. These physical tears of the plasma membrane are often repaired by
targeted exocytosis and endocytosis. Contrastingly, smaller injuries such as those generated
by electroporation and osmotic shock induce low levels of membrane disruption, tension
change and Ca2+ inux across large membrane areas. These in turn facilitate processes such as
cytoskeletal remodeling or caveolae aening. Conversely, membranes disrupted by toxic
pores do not lead to substantial increase in plane tension. As such, they can either be rapidly
shed or degraded following caveolae-mediated endocytosis. Furthermore, it appears that the
wound-healing mechanisms prevalent in a given cell-type fall not only in accordance with the
prevalence of specic injury types (i.e., PFTs vs. tears vs. ablations), but also according to cell
type-specic dierences in cell tensegrity and polarity (e.g., muscle cells vs. epithelial cells).
Similar to the plasma membrane and cytoskeletal elements interact to create tensegrity in the
single-cell scale, adhesive forces of single cells and the extracellular matrix (ECM) provide
structural stiness to tissues [1]. Considering the above, it should be no surprise that successful
single-cell repair inuences the success of tissue repair. Indeed, contrary to tissue repair, single-
cell repair is largely a binary event: it either takes place allowing the cell’s survival, or not,
leading to lysis or apoptotic removal. While relevant to wound healing at the tissue-level, these
events have lile to no relevance for single-cell wound healing outside of the modication of
the environment of other injured cells in the surrounding area (asymmetric binding, change
in ROS, Ca2+ concentration, etc.). Conversely, it seems that successful repair in one cell may
lead to an increased repair potential in surrounding cells [175, 176]. This “potentiated” repair
has been shown to involve purinergic and nitric oxide (NO)/PKG-signaling pathways [175,
176]. Similarly, repeated insults to a cell’s structural and membrane integrity presumably aect
a cell’s ability to undergo subsequent membrane resealing and cytoskeletal repair, which
would be reected in its long-term viability in a given tissue. Indeed, the prominent view of
the origin of the phenotypes associated with muscular dystrophies point toward a heighted
susceptibly to repeated mechanical wounding, leading in turn in a higher rate of single-cell
repair failure (reviewed in [177, 178]).
Another parallel between single-cell and tissue wound-healing mechanisms is their reliance
on contractile arrays. This similarity has been conrmed in multicellular models such as
Xenopus embryos [179], Caco-2 intestinal epithelial monolayers [180] and Madin-Darby canine
kidney (MDCK) epithelial monolayers [181].
Wound closure in epithelial sheets has been demonstrated to be driven by the coupling of
actomyosin contraction and collective cell migration [182–185]. The relative contribution of
each mechanism in overall re-epithelialization depends on numerous biomechanical factors,
including wound geometry [182–184], wound size [182, 186], tissue stiness [186] and ECM
composition [182]. In particular, wounds of cultured bovine corneal endothelial cell monolay-
ers in ECM-deprived conditions were observed to reseal predominantly through actomyosin
activity [182]. This is intriguing since cytoskeletal dynamics greatly inuence single-cell
wound-healing processes (see Section 3.3) and exhibits the ECM and cytoskeleton’s analogous
relationship across biological scales in the context of wound healing. These observations
How Plasma Membrane and Cytoskeletal Dynamics Influence Single-Cell Wound Healing: Mechanotransduction,
Tension and Tensegrity
http://dx.doi.org/10.5772/63765
213
suggest that the importance of tensegrity components in wound repair are conserved across
single-cell and multicellular models.
Considering the single cell’s tensegral context in future wound-healing study will help further
characterize an increasingly complex unied pathway theory of plasma membrane repair.
Author details
Eric Boucher, Tatsuya Kato and Craig A. Mandato
*
*Address all correspondence to: craig.mandato@mcgill.ca
Department of Anatomy and Cell Biology, Faculty of Medicine, McGill University, Montreal,
Quebec, Canada
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