UVB-Induced Alterations in Permeability Barrier Function: Roles for Epidermal Hyperproliferation and Thymocyte-Mediated Response

Haratake, Akinori; Uchida, Yoshikazu; Schmuth, Matthias; Tanno, Osamu; Yasuda, Rie; Epstein, John H.; Elias, Peter M.; Holleran, Walter M.

doi:10.1111/1523-1747.ep12292163

Cited by 159 publications

(155 citation statements)

References 44 publications

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“…It has been reported that chronic UVB irradiation induces an increase in TEWL in the dorsal skin of hairless mice, 8,25) but there has been no report of an increase in TEWL in the dorsal skin induced by chronic UVA irradiation in hairless mice. Bissett et al reported that when skin was UVA irradiated for 33 weeks, the TEWL was significantly increased in the 31st week compared to the level before irradiation, but it was not significantly different from TEWL in the group without UVA irradiation at the same age.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Sunscreen on Skin Elastase Activity Induced by Ultraviolet-A Irradiation

Tsukahara

Moriwaki

Hotta

et al. 2005

Biological & Pharmaceutical Bulletin

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To elucidate the mechanism underlying skin wrinkle formation, one feature of photoaging, we recently performed a study in which rat hind limb (plantar) skin was short-term chronically irradiated with ultraviolet-B (UVB) at 1 MED or lower. That study showed that elastase activity was increased in the rat hind limb skin 1) and changed the 3-dimensional structure of dermal elastic fibers, which bent the fibers responsible for skin elasticity 2,3) and thus decreased skin elasticity, forming wrinkles. 1,4,5) We also reported that this series of events could be inhibited by application of an elastase activity-inhibiting agent after UVB irradiation. 1,6,7) Inhibition of the UVB-induced increase in skin elastase activity prevented by the agent maintained the linearity of dermal elastic fibers and inhibited the decrease in skin elasticity, resulting in the inhibition of wrinkle formation. 1,6,7) This finding suggested that application of an elastase inhibitor immediately after UVB exposure would inhibit photoaging of the skin, mainly wrinkles.It has been shown that chronic UVB irradiation of the dorsal skin forms wrinkles in hairless mice 8,9) and that chronic ultraviolet-A (UVA) irradiation forms mainly sags. 8,9) In animal models, chronic UVA irradiation increased skin elastase activity and destroyed the 3-dimensional structure of dermal elastic fibers, decreasing skin elasticity, similarly to UVB irradiation.5,9-11) There have been many reports that the application of sunscreens before UV exposure inhibits the photoaging of skin in animal models and in humans. 8,[12][13][14][15][16] Based on those findings, application of a sunscreen before UV exposure might be expected to inhibit an increase in skin elastase activity even when UVA is continuously irradiated. It is therefore important and interesting to investigate the effects of chronic UVA irradiation on elastase activity in skin protected with sunscreens before irradiation in an animal model.The purpose of this study was to investigate effects of the photoprotection from UVA by topically applied sunscreens on skin elastase activity and on skin properties. MATERIALS AND METHODSAnimals Forty female HR/ICR hairless mice were used. This strain was derived by crossing 6 week old hairless mice (HR/HR) originally obtained from Nisseiken Corp (Tokyo, Japan) with the albino strain HaM/ICR. The HR/ICR strain represents a line maintained under clean conventional conditions in our laboratory by hairless brother/haired sister mating for several years. All experiments were performed with hairless female mice only, which had free access to food and water. They were housed in rooms where the lighting (without UVB emission) was automatically regulated on a 12 h light and dark cycle. The experimental protocol was approved by the Ethics Review Committee for Animal Experimentation of Kao Corp.UVA Irradiation UVA irradiation was carried out as described previously.9,10) Briefly, mice were irradiated using a bank of 12 Toshiba BL lamps with a glass filter (0.5 cm thick) for UVA (peak of...

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Section: Discussionmentioning

confidence: 99%

The Effect of Sunscreen on Skin Elastase Activity Induced by Ultraviolet-A Irradiation

Tsukahara

Moriwaki

Hotta

et al. 2005

Biological & Pharmaceutical Bulletin

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“…However, it is also clear that barrier perturbation can initiate cytokine cascades and thus influence inflammatory and mononuclear cell activation (51,52) The rapid and diffuse up-regulation of CD1d expression seen in the symptomless skin following repeated tape stripping demonstrates the highly inducible nature of CD1d expression by keratinocytes. Furthermore, a reciprocal interaction appears likely, because T cells can also influence barrier function (53). Because cytokines such as IL-1 and TNF-␣ are released after tape stripping (52), these and other cytokines are being studied to determine whether they can also induce CD1d expression by keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of CD1d by Keratinocytes in Psoriasis and CD1d-Dependent IFN-γ Production by NK-T Cells

Bonish

Jullien

Dutronc

et al. 2000

The Journal of Immunology

205

187

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The MHC class I-like protein CD1d is a nonpolymorphic molecule that plays a central role in development and activation of a subset of T cells that coexpress receptors used by NK cells (NK-T cells). Recently, T cells bearing NK receptors were identified in acute and chronic lesions of psoriasis. To determine whether NK-T cells could interact with epidermal cells, we examined the pattern of expression of CD1d in normal skin, psoriasis, and related skin disorders, using a panel of CD1d-specific mAbs. CD1d was expressed by keratinocytes in normal skin, although expression was at a relatively low level and was generally confined to upper level keratinocytes immediately beneath the lipid-rich stratum corneum. In contrast, there was overexpression of CD1d in chronic, active psoriatic plaques. CD1d could be rapidly induced on keratinocytes in normal skin by physical trauma that disrupted barrier function or by application of a potent contact-sensitizing agent. Keratinocytes displayed enhanced CD1d following exposure to IFN-γ. Combining CD1d-positive keratinocytes with human NK-T cell clones resulted in clustering of NK-T cells, and while no significant proliferation ensued, NK-T cells became activated to produce large amounts of IFN-γ. We conclude that CD1d can be expressed in a functionally active form by keratinocytes and is up-regulated in psoriasis and other inflammatory dermatoses. The ability of IFN-γ to enhance keratinocyte CD1d expression and the subsequent ability of CD1d-positive keratinocytes to activate NK-T cells to produce IFN-γ, could provide a mechanism that contributes to the pathogenesis of psoriasis and other skin disorders.

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“…Radiotherapy induced skin dermatitis exists in an acute and a chronic form [21,22]. In this study we use a high single radiation dose of 30 Gy in order to cause severe skin dermatitis.…”

Section: Discussionmentioning

confidence: 99%

“…Acute injury, which occurs within hours to weeks after radiation exposure, results from immediate structural tissue damage, generation of short-lived free radicals [24], irreversible double-stranded breaks in nuclear and mitochondrial DNA, and initiation of an inflammatory response in the epidermis and dermis [18][19][20][21]. Repeated exposure to low-dose ionizing radiation does not allow time for cells to repair DNA or tissue damage.…”

Section: Discussionmentioning

confidence: 99%

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An Innovative Complex of Benzene-Poly-Carboxylic Acid and Molybdenum, for Prevention and Treatment of Radiation Dermatitis

Fares¹

2015

Med chem

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Radiation dermatitis occurs in up to 95 percent of patients receiving radiotherapy. The aim of this study was to evaluate whether topical application of a new Benzene-Poly-Carboxylic Acid and Molybdenum Complex (BP-C2) prophylactically could protect mice skin from irradiation-induced dermatitis or treat irradiation-induced skin dermatitis, when it already has occurred. The right posterior leg of male BALB/cfC3H mice was exposed to radiation dose of 30 Gy. For prevention studies, animals were treated with BP-C2 just prior to irradiation and three times a week for 5 weeks post-radiation. For treatment studies, animals were treated with PB-C2 three times a week for five weeks when skin injury was appeared following irradiation exposure. Animals were sacrificed and skin damage was assessed using a non-linear semi-quantitative scale, as well as histological studies. Acute skin dermatitis was observed in all control animals (n=8) following 30 Gy irradiation in form of edema and ulceration grade 4. No signs of skin dermatitis were observed in the irradiated area of animals (n=8) treated with BP-C2 prior to irradiation exposure. Moreover, treatment of injured animals with BP-C2 three times a week resulted in recovery of the skin and no erythema or ulceration was hereafter observed. BP-C2 represents a potentially promising agent for prevention and treatment of irradiation-induced skin dermatitis.

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UVB-Induced Alterations in Permeability Barrier Function: Roles for Epidermal Hyperproliferation and Thymocyte-Mediated Response

Cited by 159 publications

References 44 publications

The Effect of Sunscreen on Skin Elastase Activity Induced by Ultraviolet-A Irradiation

The Effect of Sunscreen on Skin Elastase Activity Induced by Ultraviolet-A Irradiation

Overexpression of CD1d by Keratinocytes in Psoriasis and CD1d-Dependent IFN-γ Production by NK-T Cells

An Innovative Complex of Benzene-Poly-Carboxylic Acid and Molybdenum, for Prevention and Treatment of Radiation Dermatitis

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