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Peter M Elias - One of the best experts on this subject based on the ideXlab platform.
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Inducible Nitric Oxide Synthase Is Required for Epidermal Permeability Barrier Homeostasis in Mice.
Experimental dermatology, 2020Co-Authors: E. Dang, Peter M Elias, George Man, Jiechen Zhang, Dale Lee, Theodora M. Mauro, Mao-qiang ManAbstract:Nitric oxide (NO) regulates a variety of epidermal functions, including epidermal proliferation, differentiation, and cutaneous wound healing. However, whether nitric oxide (NO) and its synthetic enzymes regulate epidermal Permeability Barrier homeostasis is not clear. In the present study, we employed inducible nitric oxide synthase (iNOS) KO mice to explore the role of iNOS in epidermal Permeability Barrier homeostasis. Our results showed that iNOS mice displayed a comparable levels of basal transepidermal water loss rates, stratum corneum hydration and skin surface pH to their wild type mice, but epidermal Permeability Barrier recovery was significantly delayed both 2 and 4 hours after acute Barrier disruption by tape-stripping. In parallel, expression levels of mRNA for epidermal differentiation-related proteins and lipid synthetic enzymes were lower in iNOS KO mice versus wild type controls. Topical applications of two structurally unrelated NO donors to iNOS KO mice improved Permeability Barrier recovery kinetics, and upregulated expression levels of mRNA for epidermal differentiation-related proteins and lipid synthetic enzymes. Together, these results indicate that iNOS and its product regulate epidermal Permeability Barrier homeostasis in mice.
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A topical heparinoid-containing product improves epidermal Permeability Barrier homeostasis in mice.
Experimental dermatology, 2019Co-Authors: Ye Yao, Peter M Elias, Pan Guo, Xiaoyue Feng, Chunping Shen, Junkai Huang, Jiechen Zhang, Mao-qiang ManAbstract:Because of the importance of epidermal functions, including stratum corneum hydration and maintenance of Permeability Barrier homeostasis, in the pathogenesis of a variety of cutaneous and systemic disorders, a wide range of products has been developed to improve epidermal functions. However, the underlying mechanisms whereby certain products, including heparinoid-containing product, are far little understood. In the present study, we assessed the impact of a heparinoid-containing product, Hirudoid® cream, on epidermal Permeability Barrier function and expression levels of a panel of epidermal mRNA related to the formation/maintenance of the Permeability Barrier in mouse skin. Our results showed that while the baseline levels of transepidermal water rates remained unchanged, treatment with Hirudoid® cream twice daily for 7 days significantly accelerated Permeability Barrier recovery and increased stratum corneum hydration. In parallel, expression levels of epidermal mRNA for certain differentiation marker-related proteins, lipid synthetic enzymes, keratinocyte proliferation and antimicrobial peptides also increased significantly. Together, these results provide the underlying mechanisms by which topical Hirudoid® cream improves epidermal Permeability Barrier and antimicrobial function. Because of its benefits for epidermal functions, heparinoid-containing product could be more useful in the management of skin conditions, characterized by abnormal Permeability Barrier and antimicrobial function.
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Heavy Cigarette Smokers in a Chinese Population Display a Compromised Permeability Barrier.
BioMed research international, 2016Co-Authors: Shujun Xin, Peter M Elias, George Man, Mao-qiang ManAbstract:Cigarette smoking is associated with various cutaneous disorders with defective Permeability. Yet, whether cigarette smoking influences epidermal Permeability Barrier function is largely unknown. Here, we measured skin biophysical properties, including Permeability Barrier homeostasis, stratum corneum (SC) integrity, SC hydration, skin surface pH, and skin melanin/erythema index, in cigarette smokers. A total of 99 male volunteers were enrolled in this study. Smokers were categorized as light-to-moderate (
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Herbal medicines that benefit epidermal Permeability Barrier function
Dermatologica Sinica, 2015Co-Authors: Huibin Man, Peter M Elias, Mao-qiang ManAbstract:Epidermal Permeability Barrier function plays a critical role in regulating cutaneous functions. Hence, researchers have been searching for effective and affordable regimens to enhance epidermal Permeability Barrier function. In addition to topical stratum corneum lipids, peroxisome proliferator-activated receptor, and liver X receptor ligands, herbal medicines have been proven to benefit epidermal Permeability Barrier function in both normal and diseased skin, including atopic dermatitis, glucocorticoid-induced skin damage, and UVB-damaged skin. The potential mechanisms by which herbal medicines improve the Permeability Barrier include stimulation of epidermal differentiation, lipid production, antimicrobial peptide expression, and antioxidation. Therefore, utilization of herbal medicines could be a valuable alternative approach to enhance epidermal Permeability Barrier function in order to prevent and/or treat skin disorders associated with Permeability Barrier abnormalities.
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Therapeutic benefits of enhancing Permeability Barrier for atopic eczema
Dermatologica Sinica, 2015Co-Authors: George Man, Peter M Elias, Mao-qiang ManAbstract:Abstract The regulatory role of epidermal Permeability Barrier function in cutaneous inflammation has been well appreciated. While Barrier disruption induces cutaneous inflammation, improvement of Permeability Barrier function alleviates inflammation. Studies have demonstrated that improvement of epidermal Permeability Barrier function not only prevents the development of atopic eczema, but also delays the relapse of these diseases. Moreover, enhancing the epidermal Permeability Barrier also alleviates atopic eczema. Furthermore, co-applications of Barrier enhancing products with glucocorticoids can increase the therapeutic efficacy and reduce the adverse effects of glucocorticoids in the treatment of atopic eczema. Therefore, utilization of Permeability Barrier enhancing products alone or in combination with glucocorticoids could be a valuable approach in the treatment of atopic eczema. In this review, we discuss the benefits of improving the epidermal Permeability Barrier in the management of atopic eczema.
Kenneth R. Feingold - One of the best experts on this subject based on the ideXlab platform.
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TLR3: A Receptor that Recognizes Cell Injury Is Essential for Permeability Barrier Homeostasis Following UV Irradiation
The Journal of investigative dermatology, 2015Co-Authors: Kenneth R. FeingoldAbstract:The cutaneous Permeability Barrier is essential for life and perturbations in this Barrier are repaired rapidly. After minimal injury to the stratum corneum alterations in the calcium concentration in the outer epidermis are the primary signal inducing this repair response. In this issue, studies demonstrate that Toll-like receptor 3 has an important role in signaling Permeability Barrier repair following injury induced by UVB irradiation.
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role of lipids in the formation and maintenance of the cutaneous Permeability Barrier
Biochimica et Biophysica Acta, 2014Co-Authors: Kenneth R. Feingold, Peter M EliasAbstract:The major function of the skin is to form a Barrier between the internal milieu and the hostile external environment. A Permeability Barrier that prevents the loss of water and electrolytes is essential for life on land. The Permeability Barrier is mediated primarily by lipid enriched lamellar membranes that are localized to the extracellular spaces of the stratum corneum. These lipid enriched membranes have a unique structure and contain approximately 50% ceramides, 25% cholesterol, and 15% free fatty acids with very little phospholipid. Lamellar bodies, which are formed during the differentiation of keratinocytes, play a key role in delivering the lipids from the stratum granulosum cells into the extracellular spaces of the stratum corneum. Lamellar bodies contain predominantly glucosylceramides, phospholipids, and cholesterol and following the exocytosis of lamellar lipids into the extracellular space of the stratum corneum these precursor lipids are converted by beta glucocerebrosidase and phospholipases into the ceramides and fatty acids, which comprise the lamellar membranes. The lipids required for lamellar body formation are derived from de novo synthesis by keratinocytes and from extra-cutaneous sources. The lipid synthetic pathways and the regulation of these pathways are described in this review. In addition, the pathways for the uptake of extra-cutaneous lipids into keratinocytes are discussed. This article is part of a Special Issue entitled The Important Role of Lipids in the Epidermis and their Role in the Formation and Maintenance of the Cutaneous Barrier. Guest Editors: Kenneth R. Feingold and Peter Elias.
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Innate Immunity Stimulates Permeability Barrier Homeostasis
The Journal of investigative dermatology, 2013Co-Authors: Kenneth R. FeingoldAbstract:A key function of the skin is to provide a Permeability Barrier to restrict the movement of water, electrolytes, and other small molecules between the outside environment and the internal milieu. Following disruption of the Permeability Barrier, there is a rapid restoration of Barrier function, and one of the key signals initiating this repair response is a decrease in the concentration of calcium in the outer epidermis. In this issue, Borkowski et al. present evidence showing that activation of Toll receptor 3 by double-stranded RNA may be another pathway for activation of Permeability Barrier repair. These results provide further evidence for a link between innate immunity and the Permeability Barrier.
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Regulation of Permeability Barrier homeostasis
Clinics in dermatology, 2012Co-Authors: Kenneth R. Feingold, Mitsuhiro DendaAbstract:A major function of the skin is to provide a Barrier to the movement of water and electrolytes, which is required for life in a terrestrial environment. This Permeability Barrier is localized to the stratum corneum and is mediated by extracellular lipid-enriched lamellar membranes, which are delivered to the extracellular spaces by the secretion of lamellar bodies by stratum granulosum cells. A large number of factors have been shown to regulate the formation of this Permeability Barrier. Specifically, lamellar body secretion and Permeability Barrier formation are accelerated by decreases in the calcium content in the stratum granulosum layer of the epidermis. In addition, increased expression of cytokines and growth factors and the activation of nuclear hormone receptors (peroxisome proliferator-activated receptors, liver X receptors, vitamin D receptor) accelerate Permeability Barrier formation. In contrast, nitric oxide, protease-activated receptor 2 activation, glucocorticoids, and testosterone inhibit Permeability Barrier formation. The ability of a variety of factors to regulate Permeability Barrier formation allows for a more precise and nuanced regulation.
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IL-6 Stimulates but is not essential for stratum corneum formation and Permeability Barrier development during gestation
Experimental dermatology, 2009Co-Authors: Yan J. Jiang, Debra Crumrine, Peter M Elias, Kenneth R. FeingoldAbstract:Please cite this paper as: IL-6 Stimulates but is not essential for stratum corneum formation and Permeability Barrier development during gestation. Experimental Dermatology 2010; 19: e31–e36. Abstract: The regulation of epidermal ontogenesis is a complex process. Previous studies have shown that cytokines (IL-1, TNFα and IL-6) regulate Permeability Barrier homeostasis in adult mice. Recently, we reported that IL-1 and TNFα accelerate stratum corneum (SC) formation and Permeability Barrier development in foetal rodents. Here, we determined whether IL-6 also regulates SC formation and Permeability Barrier development during late gestation. Using a rat skin explant model, we demonstrated that IL-6 accelerates Permeability Barrier formation in a time- and dose-dependent fashion. This acceleration of Barrier formation is attributable to (a) accelerated lamellar membrane maturation, (b) formation of a multi-layer SC and (c) enhanced expression of epidermal differentiation markers. When comparing epidermis of IL-6-deficient (knockout mice) and wild-type foetal mice at days 16–18, we could not detect any abnormalities in either SC formation or the expression of differentiation markers in knockout (KO) mice. In parallel, the basal expression levels of IL-6 mRNA in epidermis and IL-6 protein in amniotic fluid were very low, with only a minimal change in IL-6 receptor mRNA levels in epidermis of days 16–22 foetal mice. These low IL-6 levels may account, at least in part, for the absence of epidermal abnormalities in IL-6 KO mice. In conclusion, exogenous IL-6 accelerates epidermal ontogenesis, but it is not essential for normal epidermal maturation.
Debra Crumrine - One of the best experts on this subject based on the ideXlab platform.
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Topical apigenin improves epidermal Permeability Barrier homoeostasis in normal murine skin by divergent mechanisms
Experimental dermatology, 2013Co-Authors: Maihua Hou, Debra Crumrine, Melanie Hupe, Theodora M. Mauro, Richard Sun, Peggy Kim, Kyungho Park, Tzu-kai Lin, Juan Luis Santiago, Peter M EliasAbstract:The beneficial effects of certain herbal medicines on cutaneous function have been appreciated for centuries. Among these agents, chrysanthemum extract, apigenin, has been used for skin care, particularly in China, for millennia. However, the underlying mechanisms by which apigenin benefits the skin are not known. In this study, we first determined whether topical apigenin positively influences Permeability Barrier homoeostasis, and then the basis thereof. Hairless mice were treated topically with either 0.1% apigenin or vehicle alone twice daily for 9 days. At the end of the treatments, Permeability Barrier function was assessed with either an electrolytic water analyzer or a Tewameter. Our results show that topical apigenin significantly enhanced Permeability Barrier homoeostasis after tape stripping, although basal Permeability Barrier function remained unchanged. Improved Barrier function correlated with enhanced filaggrin expression and lamellar body production, which was paralleled by elevated mRNA levels for the epidermal ABCA12. The mRNA levels for key lipid synthetic enzymes also were upregulated by apigenin. Finally, both cathelicidin-related peptide and mouse beta-defensin 3 immunostaining were increased by apigenin. We conclude that topical apigenin improves epidermal Permeability Barrier function by stimulating epidermal differentiation, lipid synthesis and secretion, as well as cutaneous antimicrobial peptide production. Apigenin could be useful for the prevention and treatment of skin disorders characterized by Permeability Barrier dysfunction, associated with reduced filaggrin levels and impaired antimicrobial defenses, such as atopic dermatitis.
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topical hesperidin improves epidermal Permeability Barrier function and epidermal differentiation in normal murine skin
Experimental Dermatology, 2012Co-Authors: Maihua Hou, Debra Crumrine, Peter M Elias, Melanie Hupe, Kyungho Park, M.q. Man, Wenyan Man, Wenyuan Zhu, Mao-qiang ManAbstract:Orange peel extract appears to exhibit beneficial effects on skin whitening, inflammation, UVB protection, as well as keratinocyte proliferation. In the present study, we determine whether topical hesperidin influences epidermal Permeability Barrier function and its underlying mechanisms. Hairless mice were treated topically with 2% hesperidin or 70% ethanol alone twice daily for 6 days. At the end of treatment, basal transepidermal water loss (TEWL) was measured 2 and 4 h post Barrier disruption. Epidermal proliferation and differentiation were evaluated by immunohistochemical staining and Western blot analysis. Additionally, lamellar body density and secretion were assessed by electron microscopy. Although there were no significant differences in basal Barrier function, in comparison with control animals, topical hesperidin significantly accelerated Barrier recovery at both 2 and 4 h after acute Barrier abrogation. Enhanced Barrier function in hesperidin-treated skin correlated with stimulation of both epidermal proliferation and differentiation, as well as enhanced lamellar body secretion. These results indicate that topical hesperidin enhances epidermal Permeability Barrier homeostasis at least in part due to stimulation of epidermal proliferation, differentiation, as well as lamellar body secretion.
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A topical Chinese herbal mixture improves epidermal Permeability Barrier function in normal murine skin
Experimental dermatology, 2011Co-Authors: Mao-qiang Man, Debra Crumrine, Gemma Martín-ezquerra, Melanie Hupe, D.s. Mackenzie, Carles Trullas, Seung Hun Lee, Hyun Jung Kim, Yuko Oda, Theodora M. MauroAbstract:Chinese herbal medicine (CHM) has been shown to have beneficial effects for both skin disorders with Barrier abnormality and as skin care ingredients. Yet, how CHM exerts their benefits is unclear. As most, if not all, inflammatory dermatoses are accompanied by abnormal Permeability Barrier function, we assessed the effects of topical CHM extracts on epidermal Permeability Barrier function and their potential mechanisms. Topical CHM accelerated Barrier recovery following acute Barrier disruption. Epidermal lipid content and mRNA expression of fatty acid and ceramide synthetic enzymes increased following topical CHM treatment in addition to mRNA levels for the epidermal glucosylceramide transport protein, ATP-binding cassette A12. Likewise, CHM extract increased mRNA expression of antimicrobial peptides both in vivo and in vitro. These results demonstrate that the topical CHM extract enhances epidermal Permeability Barrier function, suggesting that topical CHM could provide an alternative regimen for the prevention/treatment of inflammatory dermatoses accompanied by Barrier abnormalities.
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IL-6 Stimulates but is not essential for stratum corneum formation and Permeability Barrier development during gestation
Experimental dermatology, 2009Co-Authors: Yan J. Jiang, Debra Crumrine, Peter M Elias, Kenneth R. FeingoldAbstract:Please cite this paper as: IL-6 Stimulates but is not essential for stratum corneum formation and Permeability Barrier development during gestation. Experimental Dermatology 2010; 19: e31–e36. Abstract: The regulation of epidermal ontogenesis is a complex process. Previous studies have shown that cytokines (IL-1, TNFα and IL-6) regulate Permeability Barrier homeostasis in adult mice. Recently, we reported that IL-1 and TNFα accelerate stratum corneum (SC) formation and Permeability Barrier development in foetal rodents. Here, we determined whether IL-6 also regulates SC formation and Permeability Barrier development during late gestation. Using a rat skin explant model, we demonstrated that IL-6 accelerates Permeability Barrier formation in a time- and dose-dependent fashion. This acceleration of Barrier formation is attributable to (a) accelerated lamellar membrane maturation, (b) formation of a multi-layer SC and (c) enhanced expression of epidermal differentiation markers. When comparing epidermis of IL-6-deficient (knockout mice) and wild-type foetal mice at days 16–18, we could not detect any abnormalities in either SC formation or the expression of differentiation markers in knockout (KO) mice. In parallel, the basal expression levels of IL-6 mRNA in epidermis and IL-6 protein in amniotic fluid were very low, with only a minimal change in IL-6 receptor mRNA levels in epidermis of days 16–22 foetal mice. These low IL-6 levels may account, at least in part, for the absence of epidermal abnormalities in IL-6 KO mice. In conclusion, exogenous IL-6 accelerates epidermal ontogenesis, but it is not essential for normal epidermal maturation.
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PPARδ Activation Promotes Stratum Corneum Formation and Epidermal Permeability Barrier Development during Late Gestation
The Journal of investigative dermatology, 2009Co-Authors: Yan J. Jiang, Debra Crumrine, Peter M Elias, Matthias Schmuth, Grant D. Barish, Ronald M. Evans, Kenneth R. FeingoldAbstract:The goal of epidermal ontogenesis is to form a stratum corneum (SC), which is required for post-natal Permeability Barrier function. The regulation of epidermal ontogenesis is poorly understood, but nuclear hormone receptors have been shown to have an important function. As peroxisome proliferator-activated receptor-δ (PPARδ) is very abundant in fetal epidermis and PPARδ activation stimulates differentiation and Permeability Barrier formation in adults, we hypothesized that PPARδ might regulate epidermal ontogenesis. Treatment of fetal rat explants with the PPARδ ligand, GW 610742X, accelerates Permeability Barrier development, evidenced by a decrease in transepidermal water loss and an enhanced outside-in Barrier function, attributable to the presence of more mature lamellar membranes in the SC and enhanced expression of loricrin and involucrin. Similarly, the intra-amniotic administration of GW 610742X also accelerates the formation of the SC and Permeability Barrier development. Finally, in PPARδ-deficient mice the formation of the SC and the expression of differentiation-related proteins were delayed on days 16.5 and 17.5 of gestation. However, at later stages (day 18.5 and after birth), there were no differences between wild-type- and PPARδ-deficient mice, indicating only a transient delay in epidermal ontogenesis. These studies show that PPARδ has a role in SC formation and Permeability Barrier development.
Mao-qiang Man - One of the best experts on this subject based on the ideXlab platform.
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Inducible Nitric Oxide Synthase Is Required for Epidermal Permeability Barrier Homeostasis in Mice.
Experimental dermatology, 2020Co-Authors: E. Dang, Peter M Elias, George Man, Jiechen Zhang, Dale Lee, Theodora M. Mauro, Mao-qiang ManAbstract:Nitric oxide (NO) regulates a variety of epidermal functions, including epidermal proliferation, differentiation, and cutaneous wound healing. However, whether nitric oxide (NO) and its synthetic enzymes regulate epidermal Permeability Barrier homeostasis is not clear. In the present study, we employed inducible nitric oxide synthase (iNOS) KO mice to explore the role of iNOS in epidermal Permeability Barrier homeostasis. Our results showed that iNOS mice displayed a comparable levels of basal transepidermal water loss rates, stratum corneum hydration and skin surface pH to their wild type mice, but epidermal Permeability Barrier recovery was significantly delayed both 2 and 4 hours after acute Barrier disruption by tape-stripping. In parallel, expression levels of mRNA for epidermal differentiation-related proteins and lipid synthetic enzymes were lower in iNOS KO mice versus wild type controls. Topical applications of two structurally unrelated NO donors to iNOS KO mice improved Permeability Barrier recovery kinetics, and upregulated expression levels of mRNA for epidermal differentiation-related proteins and lipid synthetic enzymes. Together, these results indicate that iNOS and its product regulate epidermal Permeability Barrier homeostasis in mice.
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A topical heparinoid-containing product improves epidermal Permeability Barrier homeostasis in mice.
Experimental dermatology, 2019Co-Authors: Ye Yao, Peter M Elias, Pan Guo, Xiaoyue Feng, Chunping Shen, Junkai Huang, Jiechen Zhang, Mao-qiang ManAbstract:Because of the importance of epidermal functions, including stratum corneum hydration and maintenance of Permeability Barrier homeostasis, in the pathogenesis of a variety of cutaneous and systemic disorders, a wide range of products has been developed to improve epidermal functions. However, the underlying mechanisms whereby certain products, including heparinoid-containing product, are far little understood. In the present study, we assessed the impact of a heparinoid-containing product, Hirudoid® cream, on epidermal Permeability Barrier function and expression levels of a panel of epidermal mRNA related to the formation/maintenance of the Permeability Barrier in mouse skin. Our results showed that while the baseline levels of transepidermal water rates remained unchanged, treatment with Hirudoid® cream twice daily for 7 days significantly accelerated Permeability Barrier recovery and increased stratum corneum hydration. In parallel, expression levels of epidermal mRNA for certain differentiation marker-related proteins, lipid synthetic enzymes, keratinocyte proliferation and antimicrobial peptides also increased significantly. Together, these results provide the underlying mechanisms by which topical Hirudoid® cream improves epidermal Permeability Barrier and antimicrobial function. Because of its benefits for epidermal functions, heparinoid-containing product could be more useful in the management of skin conditions, characterized by abnormal Permeability Barrier and antimicrobial function.
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Heavy Cigarette Smokers in a Chinese Population Display a Compromised Permeability Barrier.
BioMed research international, 2016Co-Authors: Shujun Xin, Peter M Elias, George Man, Mao-qiang ManAbstract:Cigarette smoking is associated with various cutaneous disorders with defective Permeability. Yet, whether cigarette smoking influences epidermal Permeability Barrier function is largely unknown. Here, we measured skin biophysical properties, including Permeability Barrier homeostasis, stratum corneum (SC) integrity, SC hydration, skin surface pH, and skin melanin/erythema index, in cigarette smokers. A total of 99 male volunteers were enrolled in this study. Smokers were categorized as light-to-moderate (
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Herbal medicines that benefit epidermal Permeability Barrier function
Dermatologica Sinica, 2015Co-Authors: Huibin Man, Peter M Elias, Mao-qiang ManAbstract:Epidermal Permeability Barrier function plays a critical role in regulating cutaneous functions. Hence, researchers have been searching for effective and affordable regimens to enhance epidermal Permeability Barrier function. In addition to topical stratum corneum lipids, peroxisome proliferator-activated receptor, and liver X receptor ligands, herbal medicines have been proven to benefit epidermal Permeability Barrier function in both normal and diseased skin, including atopic dermatitis, glucocorticoid-induced skin damage, and UVB-damaged skin. The potential mechanisms by which herbal medicines improve the Permeability Barrier include stimulation of epidermal differentiation, lipid production, antimicrobial peptide expression, and antioxidation. Therefore, utilization of herbal medicines could be a valuable alternative approach to enhance epidermal Permeability Barrier function in order to prevent and/or treat skin disorders associated with Permeability Barrier abnormalities.
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Therapeutic benefits of enhancing Permeability Barrier for atopic eczema
Dermatologica Sinica, 2015Co-Authors: George Man, Peter M Elias, Mao-qiang ManAbstract:Abstract The regulatory role of epidermal Permeability Barrier function in cutaneous inflammation has been well appreciated. While Barrier disruption induces cutaneous inflammation, improvement of Permeability Barrier function alleviates inflammation. Studies have demonstrated that improvement of epidermal Permeability Barrier function not only prevents the development of atopic eczema, but also delays the relapse of these diseases. Moreover, enhancing the epidermal Permeability Barrier also alleviates atopic eczema. Furthermore, co-applications of Barrier enhancing products with glucocorticoids can increase the therapeutic efficacy and reduce the adverse effects of glucocorticoids in the treatment of atopic eczema. Therefore, utilization of Permeability Barrier enhancing products alone or in combination with glucocorticoids could be a valuable approach in the treatment of atopic eczema. In this review, we discuss the benefits of improving the epidermal Permeability Barrier in the management of atopic eczema.
Mitsuhiro Denda - One of the best experts on this subject based on the ideXlab platform.
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Regulation of Permeability Barrier homeostasis
Clinics in dermatology, 2012Co-Authors: Kenneth R. Feingold, Mitsuhiro DendaAbstract:A major function of the skin is to provide a Barrier to the movement of water and electrolytes, which is required for life in a terrestrial environment. This Permeability Barrier is localized to the stratum corneum and is mediated by extracellular lipid-enriched lamellar membranes, which are delivered to the extracellular spaces by the secretion of lamellar bodies by stratum granulosum cells. A large number of factors have been shown to regulate the formation of this Permeability Barrier. Specifically, lamellar body secretion and Permeability Barrier formation are accelerated by decreases in the calcium content in the stratum granulosum layer of the epidermis. In addition, increased expression of cytokines and growth factors and the activation of nuclear hormone receptors (peroxisome proliferator-activated receptors, liver X receptors, vitamin D receptor) accelerate Permeability Barrier formation. In contrast, nitric oxide, protease-activated receptor 2 activation, glucocorticoids, and testosterone inhibit Permeability Barrier formation. The ability of a variety of factors to regulate Permeability Barrier formation allows for a more precise and nuanced regulation.
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Phosphodiesterase inhibitors block the acceleration of skin Permeability Barrier repair by red light
Experimental dermatology, 2011Co-Authors: Makiko Goto, Sumiko Denda, Moe Tsutsumi, Kazuyuki Ikeyama, Mitsuhiro DendaAbstract:: We previously demonstrated that exposure to red light (550–670 nm) accelerates epidermal Permeability Barrier recovery after Barrier disruption. Furthermore, we showed that photosensitive proteins, originally found in retina, are also expressed in epidermis. In retina, transducin and phosphodiesterase 6 play key roles in signal transmission. In this study, we evaluate the role of phosphodiesterese 6 in the acceleration by red light of epidermal Permeability Barrier recovery. Immunohistochemical study and reverse transcription-PCR assays confirmed the expression of both transducin and phosphodiesterase 6 in epidermal keratinocytes. Topical application of 3-isobutyl-1-methylxanthine, a non-specific phosphodiesterase inhibitor, blocked the acceleration of the Barrier recovery by red light. Topical application of zaprinast, a specific inhibitor of phosphodiesterases 5 and 6, also blocked the acceleration, whereas T0156, a specific inhibitor of phosphodiesterase 5, had no effect. Red light exposure reduced the epidermal hyperplasia induced by Barrier disruption under low humidity, and the effect was blocked by pretreatment with zaprinast. Our results indicate phosphodiesterase 6 is involved in the recovery-accelerating effect of red light on the disrupted epidermal Permeability Barrier.
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Topical application of TRPM8 agonists accelerates skin Permeability Barrier recovery and reduces epidermal proliferation induced by Barrier insult: role of cold‐sensitive TRP receptors in epidermal Permeability Barrier homoeostasis
Experimental dermatology, 2010Co-Authors: Mitsuhiro Denda, Moe Tsutsumi, Sumiko DendaAbstract:TRPA1 and TRPM8 receptors are activated at low temperature (A1: below 17 degrees C and M8: below 22 degrees C). Recently, we observed that low temperature (below 22 degrees C) induced elevation of intracellular calcium in keratinocytes. Moreover, we demonstrated that topical application of TRPA1 agonists accelerated the recovery of epidermal Permeability Barrier function after disruption. In this study, we examined the effect of topical application of TRPM8 modulators on epidermal Permeability Barrier homoeostasis. Immunohistochemical study and RT-PCR confirmed the expression of TRPM8 or TRPM8-like protein in epidermal keratinocytes. Topical application of TRPM8 agonists, menthol and WS 12 accelerated Barrier recovery after tape stripping. The effect of WS12 was blocked by a non-selective TRP antagonist, Ruthenium Red, and a TRPM8-specific antagonist, BTCT. Topical application of WS12 also reduced epidermal proliferation associated with Barrier disruption under low humidity, and this effect was blocked by BTCT. Our results indicate that TRPM8 or a closely related protein in epidermal keratinocytes plays a role in epidermal Permeability Barrier homoeostasis and epidermal proliferation after Barrier insult.
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Effects of metals on skin Permeability Barrier recovery.
Experimental dermatology, 2009Co-Authors: Mitsuhiro Denda, Noriyuki KumazawaAbstract:Please cite this paper as: Effects of metals on skin Permeability Barrier recovery. Experimental Dermatology 2010; 19: e124–e127. Abstract: We previously demonstrated that the electrical state of the skin surface influences epidermal Permeability Barrier homeostasis. At the interface between different materials, electrons are localized heterogeneously and induce electrical potential. In the present study, we evaluated the effects of metals on the Barrier recovery. When we put pure gold plate on skin immediately after tape stripping, the Barrier recovery rate was faster than the control. The acceleration of Barrier recovery was blocked when the plate was earthed (grounded). When a plastic membrane was sandwiched between the plate and the skin, the recovery was delayed in comparison with the control. We then used a germanium diode to regulate the current flow between the plate and the earth. When the current was blocked, the Barrier recovery was accelerated, but when the current was not blocked, the recovery was not accelerated. These results suggest that localization of electron might affect for the Barrier recovery rate. The level of interfacial electric potential would be different due to the electrochemical property of metal. Thus, we next evaluated the effects of other metals. With samarium, zirconium, iridium and silver, the Barrier recovery rate was faster than in the case of gold, while a platinum plate induced slower recovery than in the case of gold. There was a significant correlation between work function of each metal and Barrier recovery rate. These results suggest that electron donation from outside accelerated the skin Barrier recovery.
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Paradoxical effects of β-estradiol on epidermal Permeability Barrier homeostasis
The British journal of dermatology, 2007Co-Authors: M. Tsutsumi, Mitsuhiro DendaAbstract:Summary Background Previous studies have demonstrated that sex hormones modulate epidermal Permeability Barrier homeostasis, and when the balance of these hormones is altered at menopause or during the menstrual cycle, skin sensitivity or Barrier function is changed. Objectives To observe the direct effects of sex hormones on epidermal homeostasis. Methods We examined the effects of topical application of sex hormones on Permeability Barrier recovery after tape stripping in the hairless mouse. To avoid the influence of systemic hormonal alteration, we employed male animals. Results Application of androgen (testosterone or androsterone) delayed the Barrier recovery, and the delay was overcome by co-application of β-estradiol. Progesterone also delayed the Barrier recovery, but in this case the delay was enhanced by β-estradiol. Conclusions These results suggest that changes in sex hormone balance might be associated with the skin dysfunction that often occurs during menopause, and at certain points during the menstrual cycle.