<i>Drosophila</i> as a model of wound healing and tissue regeneration in vertebrates

Belacortu, Yaiza; Paricio, Nuria

doi:10.1002/dvdy.22753

Cited by 85 publications

(97 citation statements)

References 369 publications

(371 reference statements)

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“…Movement by crawling depends on formation of lamellipodia, whereas purse-string healing is thought to, at least in part, depend on contraction of an actin/myosin cable that encircles the wounds (8,51,52). During cell crawling, forces that propel the sheet forward are generated in cells at the leading edge and in many rows behind them (3,(53)(54)(55).…”

Section: Discussionmentioning

confidence: 99%

Dual modes of motility at the leading edge of migrating epithelial cell sheets

Klarlund

2012

Proc. Natl. Acad. Sci. U.S.A.

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Purse-string healing is driven by contraction of actin/myosin cables that span cells at wound edges, and it is the predominant mode of closing small round wounds in embryonic and some adult epithelia. Wounds can also heal by cell crawling, and my colleagues and I have shown previously that the presence of unconstrained, straight edges in sheets of epithelial cells is a sufficient signal to induce healing by crawling. Here, it is reported that the presence of highly concave edges, which are free or physically constrained by an inert material (agarose), is sufficient to induce formation of purse strings. It was determined that neither of the two types of healing required cell damage or other potential stimuli by using the particularly gentle procedure of introducing gaps by digesting agarose blocks imbedded in the cell sheets. Movement by crawling depends on signaling by the EGF receptor (EGFR); however, this was not required for purse-string contraction. A migrating epithelial cell sheet usually produces finger-like projections of crawling cells. The cells between fingers contain continuous actin cables, which were also determined to contain myosin IIA and exhibit additional characteristics of purse strings. When crawling was blocked by inhibition of EGFR signaling, the concave regions continued to move, suggesting that both mechanisms contribute to propel the sheets forward. Wounding epithelial cell sheets causes activation of the EGFR, which triggers movement by crawling. The EGFR was found to be activated only at straight and convex edges, which explains how both types of movement can coexist at leading epithelial edges.

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Section: Discussionmentioning

confidence: 99%

Dual modes of motility at the leading edge of migrating epithelial cell sheets

Klarlund

2012

Proc. Natl. Acad. Sci. U.S.A.

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“…The molecular mechanism of Drosophila wound healing is highly conserved in relation to its mammalian counterpart (Li et al, 2003;Galko and Krasnow, 2004;Mace et al, 2005;Ting et al, 2005;Belacortu and Paricio, 2011), and is analogous to dorsal closure, an epithelial cell sheet movement during embryonic development (Martin and Parkhurst, 2004;Razzell et al, 2014). For re-epithelialization, JNK is the key molecule that is absolutely required although, depending on developmental stage, noncanonical components may function in the pathway (Campos et al, 2010;Lesch et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Spatiotemporal regulation of cell fusion by JNK and JAK/STAT signaling during Drosophila wound healing

Lee

Park

et al. 2017

Journal of Cell Science

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Cell-cell fusion is widely observed during development and disease, and imposes a dramatic change on participating cells. Cell fusion should be tightly controlled, but the underlying mechanism is poorly understood. Here, we found that the JAK/STAT pathway suppressed cell fusion during wound healing in the Drosophila larval epidermis, restricting cell fusion to the vicinity of the wound. In the absence of JAK/STAT signaling, a large syncytium containing a 3-fold higher number of nuclei than observed in wild-type tissue formed in wounded epidermis. The JAK/STAT ligand-encoding genes upd2 and upd3 were transcriptionally induced by wounding, and were required for suppressing excess cell fusion. JNK (also known as Basket in flies) was activated in the wound vicinity and activity peaked at ∼8 h after injury, whereas JAK/STAT signaling was activated in an adjoining concentric ring and activity peaked at a later stage. Cell fusion occurred primarily in the wound vicinity, where JAK/STAT activation was suppressed by fusion-inducing JNK signaling. JAK/ STAT signaling was both necessary and sufficient for the induction of βPS integrin (also known as Myospheroid) expression, suggesting that the suppression of cell fusion was mediated at least in part by integrin protein.

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“…Then, cells in the underlying epidermis migrate to restore epidermal continuity across the damaged area. Subsequently, these cells secrete new endocuticle on the inner surface [1][2][3][4][5][6][7]. Many mammalian tissue types, such as skin and bone, can be fully restored by tissue secretion and remodelling [8,9].…”

Section: Introductionmentioning

confidence: 99%

Bridging the gap: wound healing in insects restores mechanical strength by targeted cuticle deposition

Parle

Dirks

Taylor

2016

J. R. Soc. Interface.

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If an insect is injured, can it repair its skeleton in a manner which is mechanically strong and viable? Previous work has described the biological processes that occur during repair of insect cuticle, but until now, there has been no biomechanical assessment of the repaired area. We analysed the biomechanics of the injury repair process in the desert locust (Schistocerca gregaria). We show that after an incision, a healing process occurred which almost doubled the mechanical strength of locust tibial cuticle, restoring it to 66% of the original, intact strength. This repair process occurred by targeted cuticle deposition, stimulated by the presence of the injury. The cut surfaces remained unrepaired, but a patch of endocuticle was deposited, reinforcing the area and thus increasing the effective fracture toughness. The deposition rate of endocuticle inside the tibia increased fourfold compared with uninjured controls, but only on the dorsal side, where the incision was placed. The limb is highly loaded during jumping, so this partial restoration of strength will have a profound effect on the fitness of the insect. A finite-element model provided insights into the mechanics of the repair, predicting that the patch material reaches its ultimate strength before the fracture toughness of the existing cuticle is exceeded.

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Drosophila as a model of wound healing and tissue regeneration in vertebrates

Cited by 85 publications

References 369 publications

Dual modes of motility at the leading edge of migrating epithelial cell sheets

Dual modes of motility at the leading edge of migrating epithelial cell sheets

Spatiotemporal regulation of cell fusion by JNK and JAK/STAT signaling during Drosophila wound healing

Bridging the gap: wound healing in insects restores mechanical strength by targeted cuticle deposition

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