scholarly journals Cdc42 Deficiency Leads To Epidermal Barrier Dysfunction by Regulating Intercellular Junctions and Keratinization of Epidermal Cells during Mouse Skin Development

Theranostics ◽  
2019 ◽  
Vol 9 (17) ◽  
pp. 5065-5084 ◽  
Author(s):  
Min Zhang ◽  
Xueer Wang ◽  
Fukun Guo ◽  
Qin Jia ◽  
Nuyun Liu ◽  
...  
Keyword(s):  
Mouse Skin ◽  
Intercellular Junctions ◽  
Epidermal Cells ◽  
Barrier Dysfunction ◽  
Epidermal Barrier ◽  
Skin Development

The Impact of Ultraviolet Radiation on Barrier Function in Human Skin: Molecular Mechanisms and Topical Therapeutics

2019 ◽  
Vol 25 (40) ◽  
pp. 5503-5511 ◽  
Author(s):  
Abdulaziz Alhasaniah ◽  
Michael J. Sherratt ◽  
Catherine A. O'Neill
Keyword(s):  
Ultraviolet Radiation ◽  
Barrier Function ◽  
Molecular Mechanisms ◽  
Transepidermal Water Loss ◽  
Protective Effects ◽  
Barrier Dysfunction ◽  
Epidermal Barrier ◽  
Positive Effects ◽  
Terrestrial Mammals ◽  
The Impact

A competent epidermal barrier is crucial for terrestrial mammals. This barrier must keep in water and prevent entry of noxious stimuli. Most importantly, the epidermis must also be a barrier to ultraviolet radiation (UVR) from the sunlight. Currently, the effects of ultraviolet radiation on epidermal barrier function are poorly understood. However, studies in mice and more limited work in humans suggest that the epidermal barrier becomes more permeable, as measured by increased transepidermal water loss, in response UVR, at doses sufficiently high to induce erythema. The mechanisms may include disturbance in the organisation of lipids in the stratum corneum (the outermost layer of the epidermis) and reduction in tight junction function in the granular layer (the first living layer of the skin). By contrast, suberythemal doses of UVR appear to have positive effects on epidermal barrier function. Topical sunscreens have direct and indirect protective effects on the barrier through their ability to block UV and also due to their moisturising or occlusive effects, which trap water in the skin, respectively. Some topical agents such as specific botanical extracts have been shown to prevent the loss of water associated with high doses of UVR. In this review, we discuss the current literature and suggest that the biology of UVR-induced barrier dysfunction, and the use of topical products to protect the barrier, are areas worthy of further investigation.

scholarly journals NG2 Proteoglycan Expression in Mouse Skin: Altered Postnatal Skin Development in the NG2 Null Mouse

2007 ◽  
Vol 56 (3) ◽  
pp. 295-303 ◽  
Author(s):  
Kuniko Kadoya ◽  
Jun-ichi Fukushi ◽  
Yoshihiro Matsumoto ◽  
Yu Yamaguchi ◽  
William B. Stallcup
Keyword(s):  
Stem Cell ◽  
Mouse Skin ◽  
Hair Follicles ◽  
Stem Cell Population ◽  
Null Mouse ◽  
Outer Root Sheath ◽  
Skin Development ◽  
Bulge Region ◽  
Ng2 Proteoglycan ◽  
Stem Cell Populations

In early postnatal mouse skin, the NG2 proteoglycan is expressed in the subcutis, the dermis, the outer root sheath of hair follicles, and the basal keratinocyte layer of the epidermis. With further development, NG2 is most prominently expressed by stem cells in the hair follicle bulge region, as also observed in adult human skin. During telogen and anagen phases of the adult hair cycle, NG2 is also found in stem cell populations that reside in dermal papillae and the outer root sheaths of hair follicles. Ablation of NG2 produces alterations in both the epidermis and subcutis layers of neonatal skin. Compared with wild type, the NG2 null epidermis does not achieve its full thickness due to reduced proliferation of basal keratinocytes that serve as the stem cell population in this layer. Thickening of the subcutis is also delayed in NG2 null skin due to deficiencies in the adipocyte population.

scholarly journals The IL-13/periostin/IL-24 pathway causes epidermal barrier dysfunction in allergic skin inflammation

Allergy ◽  
2018 ◽  
Vol 73 (9) ◽  
pp. 1881-1891 ◽  
Author(s):  
Y. Mitamura ◽  
S. Nunomura ◽  
Y. Nanri ◽  
M. Ogawa ◽  
T. Yoshihara ◽  
...  
Keyword(s):  
Skin Inflammation ◽  
Barrier Dysfunction ◽  
Epidermal Barrier ◽  
Allergic Skin

scholarly journals Effect of mechanical pressure on c-fos and on the mitotic activity of epidermal cells.

1996 ◽  
Vol 43 (4) ◽  
pp. 593-601
Author(s):  
R Tsanev ◽  
J Yaneva ◽  
K Vaptzarova ◽  
D Markov
Keyword(s):  
Mitotic Cycle ◽  
Mouse Skin ◽  
State Level ◽  
Cellular Membrane ◽  
Camp Level ◽  
Epidermal Cells ◽  
Steady State Level ◽  
Camp Concentration ◽  
Mechanical Pressure ◽  
Two Peaks

A dosed mechanical pressure of 12.5 kg/cm2 applied for 1 min on depilated mouse skin did not cause cellular death or visible alterations of the cellular ultrastructures. However, it had a strong effect on the mitotic cycle of the epidermal cells-stimulating the cells to enter the mitotic cycle and temporarily blocking the G1-->S transition. This effect was strictly limited to the pressed area of the skin. The proto-oncogene c-fos was induced within the first 2 min following application of the pressure. The level of c-fos mRNA showed two peaks during the next 24 h. The first slight peak was preceded by a rapid increase in the cAMP level in the pressed skin, the second-by a fall in the cAMP concentration. A model is suggested to explain the observed effects by reversible functional damage of the cellular membrane affecting the enzymes maintaining the steady state level of cAMP.

Clinical Insights About Topical Treatment of Mild-to-Moderate Pediatric and Adult Atopic Dermatitis

2019 ◽  
Vol 23 (3_suppl) ◽  
pp. 3S-13S ◽  
Author(s):  
Charles W. Lynde ◽  
James Bergman ◽  
Loretta Fiorillo ◽  
Lyn Guenther ◽  
Jill Keddy-Grant ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Calcineurin Inhibitors ◽  
Skin Condition ◽  
Future Research ◽  
Barrier Dysfunction ◽  
Psychosocial Burden ◽  
Epidermal Barrier ◽  
Topical Corticosteroids ◽  
Topical Calcineurin Inhibitors ◽  
Inflammatory Conditions

Atopic dermatitis (AD) is a chronic inflammatory skin condition, also referred to as atopic eczema, that is identified by itching and recurrent eczematous lesions. It often starts in infancy where it affects up to 20% of children but is also highly prevalent in adults. AD inflicts a significant psychosocial burden on patients and their families and increases the risk of other immune-mediated inflammatory conditions, such as asthma and allergic rhinitis, food allergy, and mental health disorders. It is a lifelong condition associated with epidermal barrier dysfunction and altered immune function. Through the use of emollients and anti-inflammatory agents, current prevention and treatment therapies attempt to restore epidermal barrier function. Acute flares are treated with topical corticosteroids. Topical calcineurin inhibitors (TCIs) and topical corticosteroids (TCSs) are used for proactive treatment to prevent remission. There remains a need and opportunity to improve AD care through future research directed toward an improved understanding of the heterogeneity of the disease and its subtypes, the role of autoimmunity in its pathogenesis, the mechanisms behind disease-associated itch and response to specific allergens, and the comparative effectiveness and safety of therapies.

scholarly journals ALTERATION OF HISTONES FROM MOUSE EPIDERMAL CELLS AFTER INCUBATION WITH ELASTASE AND HYALURONIDASE

1971 ◽  
Vol 19 (3) ◽  
pp. 182-185 ◽  
Author(s):  
ALVIN SEGAL ◽  
MARGARET SCHROEDER ◽  
BENJAMIN L. VAN DUUREN
Keyword(s):  
Mouse Liver ◽  
Mouse Skin ◽  
Analytical Techniques ◽  
Epidermal Cells ◽  
Ultraviolet Absorption Spectrum ◽  
Tissue Preparation ◽  
Standard Procedures ◽  
Highly Sensitive ◽  
Mammalian Tissues ◽  
Liver Chromatin

Chromatin was isolated from whole mouse skin, mouse epidermal cells and mouse liver by standard procedures used for isolation of chromatin from other mammalian tissues. Chromatin from whole mouse skin or from mouse epidermal cells had not been isolated or characterized earlier. For the preparation of chromatin from mouse epidermal cells, the latter was separated from dermis by incubation for 30 min at 37°C in a solution containing the enzymes elastase and hyaluronidase. The relative proportions of the chromatin components, the T m and the ultraviolet absorption spectrum were all similar to that of chromatin from whole mouse skin which was not treated with enzymes and to other mammalian chromatin preparations. Electrophoresis of the histones from epidermal chromatin in polyacrylamide gels revealed the absence of histones F1, F3 and F2a2 and the appearance of a new band. Histones isolated from chromatin prepared from the whole mouse skin had a gel electrophoresis pattern virtually identical with histones isolated from mouse liver chromatin and to reported histone patterns from other mammalian tissues. The alterations in mouse epidermal histones are similar to reported changes in histones from calf thymus nucleohistone previously subjected to incubation at various temperatures. The enzymatic incubation technique can therefore not be used as a method of isolating unaltered mouse epidermal chromatin. The findings illustrate that very subtle chemical alterations can be induced by usual methods of tissue preparation and that these changes can only be detected by highly sensitive analytical techniques.

scholarly journals ROLE OF PROTECTIVE TOPICAL AGENTS IN THERAPY OF CHRONIC DERMATOSES

2014 ◽  
Vol 11 (3) ◽  
pp. 47-52
Author(s):  
A N KHLEBNIKOVA
Keyword(s):  
Tight Junction ◽  
Combined Therapy ◽  
Skin Barrier ◽  
Tight Junction Proteins ◽  
Barrier Dysfunction ◽  
Epidermal Barrier ◽  
Junction Proteins

Epidermal barrier insufficiency results in skin dryness and fissures in different chronic dermatoses. Barrier dysfunction is due either to genetic problems or lipid deficiency or damage of tight junction proteins. Here we discuss various abnormalities of epidermal barrier in eczema and psoriasis which necessitate to prescribe pro- tective and moisturizing agents to restore skin barrier. We give our own practice data of using Bariederm cream and balm in combined therapy of dyshidrotic eczema, plantar eczema and palmoplantar psoriasis.

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