scholarly journals A PATTERN OF EPIDERMAL CELL MIGRATION DURING WOUND HEALING

1971 ◽  
Vol 49 (2) ◽  
pp. 247-263 ◽  
Author(s):  
Walter S. Krawczyk
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Epidermal Cell ◽  
Basal Lamina ◽  
Intercellular Junctions ◽  
Mesenchymal Cells ◽  
Epidermal Cells ◽  
Model Systems ◽  
Open Wound ◽  
Electron Microscopic

Epidermal repair during wound healing is under investigation at both the light and electron microscopic levels. Suction-induced subepidermal blisters have been employed to produce two complementary model wound healing systems. These two model systems are: (a) intact subepidermal blisters, and (b) opened subepidermal blisters (the blister roof was removed immediately after induction, leaving an open wound). From these studies a pattern of movement for epidermal cells in wound healing is proposed. This pattern of movement is the same for both model systems. Epidermal cells appear to move by rolling or sliding over one another. Fine fibers oriented in the cortical cytoplasm may play an important role in the movement of these epidermal cells. Also instrumental in mediating this movement are intercellular junctions (desmosomes) and a firm attachment to a substrate through hemidesmosomes. In the intact subepidermal blisters hemidesmosomal attachment is made to a continuous and homogeneous substrate, the retained basal lamina. In the opened subepidermal blisters contact of epidermal cells is made to a discontinuous substrate composed of sporadic areas of fibrin and underlying mesenchymal cells.

scholarly journals A “traffic control” role for TGFβ3: orchestrating dermal and epidermal cell motility during wound healing

2006 ◽  
Vol 172 (7) ◽  
pp. 1093-1105 ◽  
Author(s):  
Balaji Bandyopadhyay ◽  
Jianhua Fan ◽  
Shengxi Guan ◽  
Yong Li ◽  
Mei Chen ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Epidermal Cell ◽  
Traffic Control ◽  
Transforming Growth Factor ◽  
Skin Wound ◽  
Epidermal Cells ◽  
Skin Wound Healing ◽  
Tgfβ Receptor ◽  
Dermal Cells

Cell migration is a rate-limiting event in skin wound healing. In unwounded skin, cells are nourished by plasma. When skin is wounded, resident cells encounter serum for the first time. As the wound heals, the cells experience a transition of serum back to plasma. In this study, we report that human serum selectively promotes epidermal cell migration and halts dermal cell migration. In contrast, human plasma promotes dermal but not epidermal cell migration. The on-and-off switch is operated by transforming growth factor (TGF) β3 levels, which are undetectable in plasma and high in serum, and by TGFβ receptor (TβR) type II levels, which are low in epidermal cells and high in dermal cells. Depletion of TGFβ3 from serum converts serum to a plasmalike reagent. The addition of TGFβ3 to plasma converts it to a serumlike reagent. Down-regulation of TβRII in dermal cells or up-regulation of TβRII in epidermal cells reverses their migratory responses to serum and plasma, respectively. Therefore, the naturally occurring plasma→serum→plasma transition during wound healing orchestrates the orderly migration of dermal and epidermal cells.

scholarly journals Lessons From Epithelialization: The Reason Behind Moist Wound Environment

2019 ◽  
Vol 13 (1) ◽  
pp. 34-40
Author(s):  
Sukmawati Tansil Tan ◽  
Ricky Dosan
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Cell Migration ◽  
Growth Factors ◽  
Epithelial Cells ◽  
Epidermal Cell ◽  
Major Aspect ◽  
Proliferative Phase ◽  
Wounded Area ◽  
Enhance Wound Healing

Wound healing consists of multiple structured mechanism and is influenced by various factors. Epithelialization is one of the major aspect in wound healing and inhibition of this mechanism will greatly impair wound healing. Epithelialization is a process where epithelial cells migrate upwards and repair the wounded area. This process is the most essential part in wound healing and occurs in proliferative phase of wound healing. Skin stem cells which reside in several locations of epidermis contribute in the re-epithelialization when the skin is damaged. Epithelialization process is activated by inflammatory signal and then keratinocyte migrate, differentiate and stratify to close the defect in the skin. Several theories of epithelialization model in wound healing have been proposed for decades and have shown the mechanism of epidermal cell migration during epithelialization even though the exact mechanism is still controversial. This process is known to be influenced by the wound environment where moist wound environment is preferred rather than dry wound environment. In dry wound environment, epithelialization is known to be inhibited because of scab or crust which is formed from dehydrated and dead cells. Moist wound environment enhances the epithelialization process by easier migration of epidermal cells, faster epithelialization, and prolonged presence of proteinases and growth factors. This article focuses on the epithelialization process in wound healing, epithelialization models, effects of wound environment on epithelialization and epithelialization as the basis for products that enhance wound healing.

Epidermal cell migration during wound healing in Dugesia lugubris

1984 ◽  
Vol 236 (2) ◽  
Author(s):  
Rita Pascolini ◽  
Simonetta Tei ◽  
Daniela Vagnetti ◽  
Carlo Bondi
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Epidermal Cell

Epidermal Cell Migration and Healing of the Tympanic Membrane: An Immunohistochemical Study of Cell Proliferation Using Bromodeoxyuridine Labeling

1995 ◽  
Vol 104 (3) ◽  
pp. 218-225 ◽  
Author(s):  
Reiko Koba
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Tympanic Membrane ◽  
Epidermal Cell ◽  
Immunohistochemical Study ◽  
Epidermal Cells ◽  
Brdu Injection ◽  
Mucosal Cells ◽  
Epidermal Cell Proliferation ◽  
Perforated Tympanic Membrane

A monoclonal antibody against bromodeoxyuridine (BrdU) was used to investigate cell proliferation in the tympanic membrane of white rabbits. The BrdU-labeled cells were observed mainly in the epidermis of the annulus, around the malleus handle, and in the anterior and posterior superior quadrants of the normal rabbit tympanic membrane at 2 hours after BrdU injection. At 5 days the localization of the BrdU-labeled cells had changed centrifugally from the malleus handle toward the annulus. This change in the distribution of BrdU-labeled cells suggested that epidermal cell migration is caused by cell proliferation and insertion of newly proliferated epidermal cells at the proliferation center. Immunohistochemical observation of BrdU-labeled cells in the artificially perforated tympanic membrane suggested that the process of healing of the perforation may be as follows. Epidermal cell proliferation in the whole tympanic membrane is accelerated by the perforation stimulus. Then the proliferated epidermal cells migrate to the edge of the perforation. In contrast, proliferation of connective tissue cells and mucosal cells is stimulated only around the perforation, and cooperates with the proliferated epidermal cells to close the perforation.

scholarly journals Expression of the Alternative Oxidase Influences Jun N-Terminal Kinase Signaling and Cell Migration

2018 ◽  
Vol 38 (24) ◽  
Author(s):  
Ana Andjelković ◽  
Amelia Mordas ◽  
Lyon Bruinsma ◽  
Annika Ketola ◽  
Giuseppe Cannino ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Heat Production ◽  
Alternative Oxidase ◽  
Electron Flow ◽  
Model Systems ◽  
Jnk Pathway ◽  
Jnk Signaling ◽  
Content Type ◽  
Pathway Inhibition

ABSTRACTDownregulation of Jun N-terminal kinase (JNK) signaling inhibits cell migration in diverse model systems. InDrosophilapupal development, attenuated JNK signaling in the thoracic dorsal epithelium leads to defective midline closure, resulting in cleft thorax. Here we report that concomitant expression of theCiona intestinalisalternative oxidase (AOX) was able to compensate for JNK pathway downregulation, substantially correcting the cleft thorax phenotype. AOX expression also promoted wound-healing behavior and single-cell migration in immortalized mouse embryonic fibroblasts (iMEFs), counteracting the effect of JNK pathway inhibition. However, AOX was not able to rescue developmental phenotypes resulting from knockdown of the AP-1 transcription factor, the canonical target of JNK, nor its targets and had no effect on AP-1-dependent transcription. The migration of AOX-expressing iMEFs in the wound-healing assay was differentially stimulated by antimycin A, which redirects respiratory electron flow through AOX, altering the balance between mitochondrial ATP and heat production. Since other treatments affecting mitochondrial ATP did not stimulate wound healing, we propose increased mitochondrial heat production as the most likely primary mechanism of action of AOX in promoting cell migration in these various contexts.

Cell polarity during wound healing in an insect epidermis

Development ◽  
1987 ◽  
Vol 100 (1) ◽  
pp. 163-170 ◽  
Author(s):  
K. Nubler-Jung ◽  
R. Bonitz ◽  
M. Sonnenschein
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Cell Movement ◽  
Epidermal Cells ◽  
Time Interval ◽  
Directed Cell Migration ◽  
Cell Components ◽  
Insect Epidermis ◽  
Insect Integument ◽  
Would Healing

The insect integument displays uniform posterior orientation of cuticular denticles or bristles formed by the epidermal cells. We want to understand how cell polarities become uniformly oriented in the plane of the epidermal sheet. Here we test whether directed cell migration disturbs the orientation of denticles. Burning a circular area of epidermal cells beneath the cuticle causes cells to migrate into the resulting wound and the cuticle pattern observed after the subsequent moult depends on the time interval between burning and ecdysis. After a short wound-healing period cuticular protrusions tend to point away from the wound. With increasing would healing periods they tend to point more and more towards the wound centre. These results suggest that the migrating cells tend to orient cuticular protrusions in the direction of cell movement while continued cell movement will bend nascent cuticular protrusions outwards. Cell shape may also determine denticle orientation. I propose that the asymmetric localization of cell components known to determine the orientation of cell migration may also determine denticle orientation in insect epidermal cells.

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