E‐cadherin expression in wound healing of mouse skin

Kuwahara, Masamitsu; Hatoko, Mitsuo; Tada, Hideyuki; Tanaka, Aya

doi:10.1034/j.1600-0560.2001.028004191.x

Cited by 45 publications

(37 citation statements)

References 12 publications

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“…Cyto-8 and E-cad proteins are produced by both mouse and human keratinocytes [25,26]. Cyto-8 functions to maintain structural integrity, indicates epithelial differentiation and characterizes malignancy of tumors [27], while E-cad up-regulates the adherent properties in keratinocytes and melanocytes as well as cancerous cells like melanoma [8,12,28–30].…”

Section: Resultsmentioning

confidence: 99%

The use of an in vitro 3D melanoma model to predict in vivo plasmid transfection using electroporation

Marrero

Heller

2012

Biomaterials

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A large-scale in vitro 3D tumor model was generated to evaluate gene delivery procedures in vivo. This 3D tumor model consists of a “tissue-like” spheroid that provides a micro-environment supportive of melanoma proliferation, allowing cells to behave similarly to cells in vivo. This functional spheroid measures approximately 1 cm in diameter and can be used to effectively evaluate plasmid transfection when testing various electroporation (EP) electrode applicators. In this study, we identified EP conditions that efficiently transfect green fluorescent protein (GFP) and interleukin 15 (IL-15) plasmids into tumor cells residing in the 3D construct. We found that plasmids delivered using a 6-plate electrode applying 6 pulses with nominal electric field strength of 500 V/cm and pulse-length of 20 ms produced significant increase of GFP (7.3-fold) and IL-15 (3.0–fold) expression compared to controls. This in vitro 3D model demonstrates the predictability of cellular response toward delivery techniques, limits the numbers of animals employed for transfection studies, and may facilitate future developments of clinical trials for cancer therapies in vivo.

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Section: Resultsmentioning

confidence: 99%

The use of an in vitro 3D melanoma model to predict in vivo plasmid transfection using electroporation

Marrero

Heller

2012

Biomaterials

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“…A hallmark of successful wound repair is the reestablishment of cell : cell junctions and barrier function, thereby illustrating dynamic modulation of adherens junctions and desmosomes during wound reepithelialization. In mouse epidermis, a decrease in E-cadherin is evident 3 days after wounding in full-thickness incisional or excisional wound models with subsequent protein restoration upon wound closure [5]. Blocking E-cadherin function with antibody caused uneven wound margins and disruption of the reorganizing actin cytoskeleton in mouse epidermis [6], demonstrating the importance of E-cadherin in wound repair.…”

Section: Introductionmentioning

confidence: 99%

Differential Downregulation of E-Cadherin and Desmoglein by Epidermal Growth Factor

Chavez

Buhr

Petrie

et al. 2012

Dermatology Research and Practice

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Modulation of cell : cell junctions is a key event in cutaneous wound repair. In this study we report that activation of the epidermal growth factor (EGF) receptor disrupts cell : cell adhesion, but with different kinetics and fates for the desmosomal cadherin desmoglein and for E-cadherin. Downregulation of desmoglein preceded that of E-cadherin in vivo and in an EGF-stimulated in vitro wound reepithelialization model. Dual immunofluorescence staining revealed that neither E-cadherin nor desmoglein-2 internalized with the EGF receptor, or with one another. In response to EGF, desmoglein-2 entered a recycling compartment based on predominant colocalization with the recycling marker Rab11. In contrast, E-cadherin downregulation was accompanied by cleavage of the extracellular domain. A broad-spectrum matrix metalloproteinase inhibitor protected E-cadherin but not the desmosomal cadherin, desmoglein-2, from EGF-stimulated disruption. These findings demonstrate that although activation of the EGF receptor regulates adherens junction and desmosomal components, this stimulus downregulates associated cadherins through different mechanisms.

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“…E-cadherin expression decreases close to the edge of a wound, potentially allowing cells to lose cell-cell adhesion, migrate and increase proliferation (Fig. 4C; Kuwahara et al 2001). The transcription factor COUP-TF interacting protein 2 is required for migration, and down-regulation of E-cadherin expression (Liang et al 2012).…”

Section: Epidermis Organization and Regulation Of Homeostasismentioning

confidence: 99%

Cell–Cell Junctions Organize Structural and Signaling Networks

García

Nelson

Chavez

2017

Cold Spring Harb Perspect Biol

312

221

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Cell-cell junctions link cells to each other in tissues, and regulate tissue homeostasis in critical cell processes that include tissue barrier function, cell proliferation and migration. Defects in cell-cell junctions give rise to a wide range of tissue abnormalities that disrupt homeostasis and are common in genetic abnormalities and cancers. Here, we discuss the organization and function of cell-cell junctions primarily involved in adhesion (Tight Junction, Adherens Junction, and Desmosomes) in two different epithelial tissues: a simple epithelium (intestine) and a stratified epithelium (epidermis). Studies in these tissues reveal similarities and differences in the organization and functions of different cell-cell junctions that meet the requirements for the specialized functions of each tissue. We discuss cell-cell junction responses to genetic and environmental perturbations that provide further insights into their roles in maintaining tissue homeostasis.

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E‐cadherin expression in wound healing of mouse skin

Abstract: The results suggested that E-cadherin expression decreases in epithelial cells. This decrease may depend on the activity of migration and mitosis. In addition, the change was similar in both the excisional and incisional wounds.

Cited by 45 publications

References 12 publications

The use of an in vitro 3D melanoma model to predict in vivo plasmid transfection using electroporation

The use of an in vitro 3D melanoma model to predict in vivo plasmid transfection using electroporation

Differential Downregulation of E-Cadherin and Desmoglein by Epidermal Growth Factor

Cell–Cell Junctions Organize Structural and Signaling Networks

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