The epithelial reaction in the healing of excised cutaneous wounds in the dog

Winstanley, E. W.

doi:10.1016/0021-9975(75)90085-7

Cited by 19 publications

(9 citation statements)

References 8 publications

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“…1, compare D and E). As reported previously (e.g., Odland and Ross, 1968;Winstanley, 1975), many spinous keratinocytes featured membrane-bound vacuoles in their cytoplasm ( Fig. 1 E), and the intercellular spaces were considerably enlarged.…”

Section: The Accumulation Of K6 Ki6 and K17 At The Wound Edge Corresupporting

confidence: 87%

Onset of re-epithelialization after skin injury correlates with a reorganization of keratin filaments in wound edge keratinocytes: defining a potential role for keratin 16.

Paladini

Takahashi

Bravo

et al. 1996

The Journal of Cell Biology

370

384

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Abstract. Injury to stratified epithelia causes a strong induction of keratins 6 (K6) and 16 (K16) in post-mitotic keratinocytes located at the wound edge. We show that induction of K6 and K16 occurs within 6 h after injury to human epidermis. Their subsequent accumulation in keratinocytes correlates with the profound reorganization of keratin filaments from a pan-cytoplasmic distribution to one in which filaments are aggregated in a juxtanuclear location, opposite to the direction of cell migration. This filament reorganization coincides with additional cytoarchitectural changes and the onset of re-epithelialization after 18 h post-injury. By following the assembly of K6 and K16 in vitro and in cultured cells, we find that relative to K5 and K14, a well-characterized keratin pair that is constitutively expressed in epidermis, K6 and K16 polymerize into short 10-nm filaments that accumulate near the nucleus, a property arising from K16. Forced expression of human K16 in skin keratinocytes of transgenic mice causes a retraction of keratin filaments from the cell periphery, often in a polarized fashion. These results imply that K16 may not have a primary structural function akin to epidermal keratins. Rather, they suggest that in the context of epidermal wound healing, the function of K16 could be to promote a reorganization of the cytoplasmic array of keratin filaments, an event that precedes the onset of keratinocyte migration into the wound site. ~]~ typical stratified squamous epithelium, the epidermis shows a polarity in its functional organization and morphology. This polarity reflects the maintenance of an optimal balance between proliferation and differentiation, such that this self-renewing tissue maintains an architecture that is ideal for a barrier function. Progenitor cells reside in the basal layer, where keratinocytes are mitotically active, have a low columnar shape, appear relatively undifferentiated, and express specific markers such as the type II keratin K5 and type I keratins K14 (Nelson and Sun, 1983). Upon commitment to differentiation, basal keratinocytes exit the cell cycle and migrate upward to the suprabasal compartment (Fuchs, 1993). This commitment triggers a specific program of gene expression during which suprabasal keratinocytes steadily progress towards a cytoarchitecture in which they are completely flattened, have lost their organelles and nucleus, and have most of their protein content covalently cross-linked via the action of transglutaminases (Rice and Green, 1979). It is believed that commitment to terminal differentiation, which is accompanied by a switch in keratin gene expression from

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Section: The Accumulation Of K6 Ki6 and K17 At The Wound Edge Corresupporting

confidence: 87%

Onset of re-epithelialization after skin injury correlates with a reorganization of keratin filaments in wound edge keratinocytes: defining a potential role for keratin 16.

Paladini

Takahashi

Bravo

et al. 1996

The Journal of Cell Biology

370

384

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“…Re-epithelialization starts approximately 16-24 h after injury during the proliferation phase, and continues over the second and third phase of the wound healing process [11,[21][22][23][24][25][26]. Upon acute skin injury, neutrophils, monocytes, and macrophages are recruited to the site of injury when the barrier is disrupted [27].…”

Section: Wound Re-epithelializationmentioning

confidence: 99%

Re-epithelialization of adult skin wounds: Cellular mechanisms and therapeutic strategies

Rousselle

Braye

Dayan

2019

Advanced Drug Delivery Reviews

370

278

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Cutaneous wound healing in adult mammals is a complex multi-step process involving overlapping stages of blood clot formation, inflammation, re-epithelialization, granulation tissue formation, neovascularization, and remodelling. Re-epithelialization describes the resurfacing of a wound with new epithelium. The cellular and molecular processes involved in the initiation, maintenance, and completion of epithelialization are essential for successful wound closure. A variety of modulators are involved, including growth factors, cytokines, matrix metalloproteinases, cellular receptors, and extracellular matrix components. Here, we focus on cellular mechanisms underlying keratinocyte migration and proliferation during epidermal closure. Inability to re-epithelialize is a clear indicator of chronic non-healing wounds, which fail to proceed through the normal phases of wound healing in an orderly and timely manner. This review summarizes the current knowledge regarding the management and treatment of acute and chronic wounds, with a focus on re-epithelialization, offering some insights into novel future therapies.

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“…In the 'rolling mechanism', the leading cells are successively implanted as new basal cells, and other cells roll over these (Krawczyk 1971;Winstanley 1975;Ortonne et al 1981). In the 'sliding mechanism', on the other hand, the cells in the interior of the sheet respond passively to the pull of the marginal cells.…”

Section: Biological Backgroundmentioning

confidence: 99%

Mathematical analysis of a basic model for epidermal wound healing

1991

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The stimuli for the increase in epidermal mitosis during wound healing are not fully known. We construct a mathematical model which suggests that biochemical regulation of mitosis is fundamental to the process, and that a single chemical with a simple regulatory effect can account for the healing of circular epidermal wounds. The numerical results of the model compare well with experimental data. We investigate the model analytically by making biologically relevant approximations. We then obtain travelling wave solutions which provide information about the accuracy of these approximations and clarify the roles of the various model parameters.

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The epithelial reaction in the healing of excised cutaneous wounds in the dog

Cited by 19 publications

References 8 publications

Onset of re-epithelialization after skin injury correlates with a reorganization of keratin filaments in wound edge keratinocytes: defining a potential role for keratin 16.

Onset of re-epithelialization after skin injury correlates with a reorganization of keratin filaments in wound edge keratinocytes: defining a potential role for keratin 16.

Re-epithelialization of adult skin wounds: Cellular mechanisms and therapeutic strategies

Mathematical analysis of a basic model for epidermal wound healing

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