Acute Photodamage Research Articles

How to fight acute sun damage? Current skin care strategies

Excessive exposure to sunlight can contribute for skin photo-damage, such as sunburn, dryness, wrinkles, hyperpigmentation, immunosuppressive events and skin sensitization reactions. The use of aftersun products is an effective strategy to reduce the visible signs and symptoms of acute photodamage in the skin. Aiming to unveil the active ingredients able to offset acute sun damage, this work focuses on the characterization of the aftersun products market. A total of 84 after-sun formulations from 41 international brands currently marketed in Portugal were analyzed concerning the composition described on the product label, identifying natural and synthetic/semi-synthetic ingredients with the ability to mitigate solar-induced effects. The majority of aftersun formulations contained ingredients derived from terrestrial and marine sources (> 80%). An in-depth examination of these compounds is also offered, revealing the top of the most used natural and synthetic/semi-synthetic ingredients present in aftersun products, as well as their mechanism of action. A critical appraisal of the scientific data was made aiming to highlight the scientific evidence of ingredients able to mitigate skin photodamage. Amino acids and peptides, and A. barbadensis extract were tested for their in vivo efficacy. Nevertheless, all the ingredients were analyzed with in vitro studies as preliminary screening before in vivo, ex vivo and/or clinical studies. In summary, this study provides an overview of the use of active ingredients in commercial aftersun products to understand better the benefits associated with their use in cosmetic formulations and identify opportunities for innovation.Graphical abstract

High molecular weight hyaluronic acid-liposome delivery system for efficient transdermal treatment of acute and chronic skin photodamage

Photodamage is one of the most common causes of skin injury. High molecular weight hyaluronic acid (HHA) has shown immense potential in the treatment of skin photodamage by virtue of its anti-inflammatory, reparative, and antioxidative properties. However, due to its large molecular structure of HHA, HHA solution could only form a protective film on the skin surface in conventional application, failing to effectively penetrate the skin, which necessitates the development of new delivery strategies. Liposomes, with a structure similar to biological membranes, have garnered extensive attention as transdermal drug delivery carriers because of their advantages in permeability, dermal compatibility, and biosafety. Herein, we have developed a HHA-liposome transdermal system (HHL) by embedding HHA into the liposome structure using reverse evaporation, high-speed homogenization, and micro-jet techniques. The effective penetration and long-term residence of HHA in skin tissue were multidimensionally verified, and the kinetics of HHA in the skin were extensively studied. Moreover, it was demonstrated that HHL significantly strengthened the activity of human keratinocytes and effectively inhibits photo-induced cellular aging in vitro. Furthermore, a murine model of acute skin injury induced by laser ablation was established, where the transdermal system showed significant anti-inflammatory and immunosuppressive properties, promoting skin proliferation and scar repair, thereby demonstrating immense potential in accelerating skin wound healing. Meanwhile, HHL significantly ameliorated skin barrier dysfunction caused by simulated sunlight exposure, inhibited skin erythema, inflammatory responses, and oxidative stress, and promoted collagen expression in a chronic photodamage skin model. Therefore, this transdermal delivery system with biocompatibility represents a promising new strategy for the non-invasive application of HHA in skin photodamage, revealing the significant potential for clinical translation and broad application prospects. Statement of significanceThe transdermal system utilizing hyaluronic acid-based liposomes enhances skin permeability and retains high molecular weight hyaluronic acid (HHL). In vitro experiments with human keratinocytes demonstrate significant skin repair effects of HHL and its effective inhibition of cellular aging. In an acute photodamage model, HHL exhibits stronger anti-inflammatory and immunosuppressive properties, promoting skin proliferation and scar repair. In a chronic photodamage model, HHL significantly improves skin barrier dysfunction, reduces oxidative stress induced by simulated sunlight, and enhances collagen expression.

Rapamycin protects mouse skin from ultraviolet B-induced photodamage by modulating Hspb2-mediated autophagy and apoptosis.

Continuous exposure to UVB is the main extrinsic cause of skin photodamage, which is associated with oxidative stress, DNA damage, apoptosis and degradation of collagen. Rapamycin, a mechanistic target inhibitor of rapamycin complex 1 (mTORC1), has been shown to play a crucial role anti-tumor and aging retardation, but its mechanism of action in UVB-induced photodamage still remains unknown. In this study, we investigated the role of rapamycin and Hspb2 (also known as Hsp27) in UVB-induced photodamage in mice. We constructed skin acute photodamage models on the ears of WT and Hspb2 KO mice, respectively, and administered rapamycin treatment. Histological results showed that knockout of the hspb2 exacerbated the skin damage, as evidenced by thickening of the epidermis, breakage and disruption of collagen fibers and reduction in their number, which is reversed by rapamycin treatment. In addition, hspb2 knockout promoted UVB-induced apoptosis and reduced autophagy levels, with a significant increase in p53 levels and Bax/Bcl-2 ratio, a reduction in LC3II/I ratio and an increase in p62 levels in the KO mice compared to those in WT mice after the same dose of UVB irradiation. Rapamycin was also found to inhibit collagen degradation induced by hspb2 knockdown through activation of the TGF-β/Smad signaling pathway. Rapamycin can alleviate skin photodamage from Hspb2 knockout to some extent. It may be a potential therapeutic drug for skin photodamage. In this study, we investigated the role of rapamycin and Hspb2 in UVB-induced photodamage in mice. Histological results showed that knockout of the hspb2 exacerbated the skin damage, as evidenced by thickening of the epidermis, breakage and disruption of collagen fibers and reduction in their number, which is reversed by rapamycin treatment. In addition, hspb2 knockout promoted UVB-induced apoptosis and reduced autophagy levels. Rapamycin was also found to inhibit collagen degradation induced by hspb2 knockdown through activation of the TGF-β/Smad signaling pathway. We conclude that rapamycin and Hspb2 exert a synergistic protective effect in skin photodamage.

Dendrobium nobile Lindl Polysaccharides Attenuate UVB-induced Photodamage by Regulating Oxidative Stress, Inflammation and MMPs Expression in Mice Model.

Acute ultraviolet B (UVB) irradiation predominantly leads to various skin disorders caused by photodamage. The major causes of UVB-induced photodamage include oxidative stress, inflammatory infiltration and collagen degradation. The aim of the study was to elucidate whether DNP had protective effect on the skin of KM mice when exposed to UVB irradiation. The DNP protective properties to skin appearance and histopathological alterations in KM mice were evaluated by hematoxylin-eosin staining, toluidine blue staining, Gomori staining and Masson's trichrome staining and mast cell staining. In this study, DNP pretreatment promoted the activities of antioxidant enzymes, including superoxide dismutase, catalase and glutathione peroxidase, while decreased malondialdehyde level in UVB-irradiated skin, along with downregulation of proteins expression of matrix metalloproteinases and reduction in the level of the proinflammatory cytokines. Based on these findings, we demonstrated that DNP displayed strong ameliorative effects on UVB-induced acute photodamage for the first time, indicating that it would be a promoting ingredient candidate that could be used in antiphotodamage.

Applying sunscreen SPF 50 with high antioxidant capacity during fifteen days improves the dermis echogenicity and reduces the reddish skin undertone.

Of the many effects induced by UV radiation on the skin, erythema is one of the most well-known features, which is a cutaneous inflammatory reaction correlated with acute photodamage. The utilization of sunscreen may reduce this process. To evaluate the utilization of a sunscreen SPF50 with high antioxidant capacity during 15 days by young men without photoprotection habits. For this, we evaluated erythema, skin hydration properties, and dermis echogenicity using skin imaging techniques. Forty male participants (aged between 18 and 28 years old), 36 without previous photoprotection habits, were recruited, and the erythema was evaluated using a visual score and skin colorimeter. Macroscopic images (VivaCam®) were also obtained. Dermis echogenicity was evaluated using high-frequency ultrasonography. All the participants received a sunscreen SPF 50 to use for 15 days. The visual score presented a strong correlation (r=0.8657) with the colorimeter results. Visually and using the biophysical methodologies was possible to observe the reduction of the visual erythema. The dermis echogenicity also improved, probably correlated with the acute inflammation reduction. No alterations were observed in the skin hydration and skin barrier parameters. The utilization of complementary and correlated different skin biophysical and imaging techniques in this study allows a better comprehension regarding the skin early photoaging process due the direct sun exposure. The utilization with a SPF 50 sunscreen with high antioxidant potential allows for a reduction in the erythema after 15 days of usage, a quick result, however, did not improved the skin barrier or SC hydration.

Anti-inflammation and anti-aging mechanisms of mercaptopurine in vivo and in vitro

Skin is the biggest organ of the human body, which easily gets irritated by exposure to the sun. Skin photoaging and acute photodamage are caused by intense UV-B radiation. Therefore, it is imperative to find new compounds to prevent skin damage and aging. Mercaptopurine is an immunologic agent commonly used for treating Acute lymphoblastic leukemia and inflammatory bowel disease. The beneficial effects of mercaptopurine on the skin have not been reported, and its intrinsic mechanism of action is unclear. Therefore, this study was to explore mercaptopurine when exposed to UV-B radiation in HacaT cells and C57BL6 mice aging and damage effects. The model of in vivo UV-B-induced skin damage and skin photoaging was established, and the impact of mercaptopurine on cell and animal skin was studied. The study found that mercaptopurine, on the one hand, inhibits cellular and animal senescence. On the other, it inhibits the expression of mitogen-activated protein kinase (MAPK) and the nuclear factor κB (NF-κB), which are important signaling molecules in the early UV-B reaction signaling pathway. In addition, mercaptopurine downregulates matrix metalloproteinase expression, increases collagen fiber content, and facilitates collagen synthesis. Treatment with mercaptopurine also inhibits the expression of inflammatory factors and reduces inflammatory cell infiltration of the skin. In conclusion, our study elucidates mercaptopurine's anti-photoaging and anti-inflammatory activity in cellular and animal models.

Conditioned Medium from H2O2-Preconditioned Human Adipose-Derived Stem Cells Ameliorates UVB-Induced Damage to Human Dermal Fibroblasts.

Human skin exposure to ultraviolet B (UVB) radiation can result in acute photodamage through oxidative modifications of cellular components and biomolecules involved in the metabolism of dermal cells. Recently, the therapeutic potential of human adipose-derived stem cells (hASCs) has been investigated as a novel strategy for photoprotection due to their pro-angiogenic properties, protective activity against oxidative stress and paracrine effect on dermal cells. To enhance these therapeutic properties, hASCs can be preconditioned by exposing them to sublethal cellular stressors. In this study, we first analyzed response capacity against UVB-induced oxidative stress in H2O2-preconditioned hASCs (called HC016 cells); and second, we evaluated the photoprotective effect of HC016-conditioned medium (CM) in an in vitro UVB irradiation model in cultured human foreskin fibroblasts (hFFs). The results demonstrated that HC016 cells have a greater capacity to respond efficiently to UVB-induced oxidative stress, evidenced by higher Nrf2 antioxidant system activity and enhanced viability and migration capacity. Further, HC016-CM treatment increased viability, migratory capacity and collagen type I synthesis in hFFs exposed to UVB radiation, as well as reducing their cytotoxicity, apoptosis, senescence and IL-6 secretion. Collectively, these findings support the view that HC016 cells could protect against UVB-induced photodamage via paracrine mechanisms.

Frog Skin Derived Peptides With Potential Protective Effects on Ultraviolet B-Induced Cutaneous Photodamage.

Hyla annectans is a tree frog living in the southwestern plateau area of China where there is strong ultraviolet radiation and long duration of sunshine. So their naked skin may possess chemical defense components that protect it from acute photo-damage. However, no such peptide or components has been identified till to date. In the current work, two novel peptides (FW-1, FWPLI-NH2 and FW-2, FWPMI-NH2) were identified from the skin of the tree frog. Five copies of FW-1 and four copies of FW-2 are encoded by an identical gene and released from the same protein precursor, which possess 167 amino acid residues. FW-1 and -2 can exert significant anti-inflammatory functions by directly inhibiting Ultraviolet B irradiation (UVB)-induced secretion of inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). They may achieve this function by modulating the UV-induced stress signaling pathways such as Mitogen-activated protein kinases (MAPK) and Nuclear Factor Kappa B (NF-κB). Besides, FW-1 and -2 showed potential antioxidant effects on epidermis by attenuating the UVB-induced reactive oxygen species (ROS) production through an unknown mechanism. Considering small peptides’ easy production, storage, and potential photo-protective activity, FW-1/2 might be exciting leading compounds or templates for the development of novel pharmacological agents for the suppression of UVB-induced skin inflammation. Moreover, this study might expand our knowledge on skin defensive mechanism of tree frog upon UVB irradiation.

N-Terminal 5-Mer Peptide Analog P165 of Amyloid Precursor Protein Repairs Skin Photodamage Induced by UVB through the Nrf2 Signaling Pathway.

Background:Acute photodamage is an acute inflammatory reaction of the skin after ultraviolet (UV) irradiation. Many drugs have been successfully used for the treatment and prevention of photodamage.Aims:To evaluate the molecular mechanism of N-terminal 5-mer peptide analog P165 of amyloid precursor protein in repairing photodamaged rat skin.Materials and Methods:We establish a rat model of acute UVB photodamage. The ratskin was treated with or without 250, 500, and, 1000 μM P165. Histological analysis was performed by hematoxylin and eosin staining. Apoptotic cells were analyzed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The kits were used to measure the levels of protein carbonyl (PC), malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH). Western blotting was used to measure Nrf2.Results:P165 repaired UVB-induced cutaneous erythema and edema, and reduced apoptosis of skin cells. The levels of PC, MDA, and 8-OHdG in 250 and 500 μM P165 groups were all lower than those in the solvent group. Activities of SOD, CAT, and GPx, and the level of GSH in P165 groups were higher than those in the solvent group. Nrf2 expression in the solvent group was higher than that in the negative group, whereas in the 500 μM P165 group was higher than in the solvent group.Conclusions:Our findings suggest that P165 repairs the rat skin with acute photodamage by reducing oxidative stress. These activities may be mediated by promoting the Nrf2 signaling pathway. Thus, P165 may be a promising agent for the treatment of acute photodamage, which may be used in cosmetics and postsun repair.

Retracted: Protective Effects of Soy Oligopeptides in Ultraviolet B-Induced Acute Photodamage of Human Skin.

[This retracts the article DOI: 10.1155/2016/5846865.].

Preclinical pharmacology of a lipophenol in a mouse model of light-induced retinopathy

Environmental light has deleterious effects on the outer retina in human retinopathies, such as ABCA4-related Stargardt’s disease and dry age-related macular degeneration. These effects involve carbonyl and oxidative stress, which contribute to retinal cell death and vision loss. Here, we used an albino Abca4−/− mouse model, the outer retina of which shows susceptibility to acute photodamage, to test the protective efficacy of a new polyunsaturated fatty acid lipophenol derivative. Anatomical and functional analyses demonstrated that a single intravenous injection of isopropyl-phloroglucinol-DHA, termed IP-DHA, dose-dependently decreased light-induced photoreceptor degeneration and preserved visual sensitivity. This protective effect persisted for 3 months. IP-DHA did not affect the kinetics of the visual cycle in vivo or the activity of the RPE65 isomerase in vitro. Moreover, IP-DHA administered by oral gavage showed significant protection of photoreceptors against acute light damage. In conclusion, short-term tests in Abca4-deficient mice, following single-dose administration and light exposure, identify IP-DHA as a therapeutic agent for the prevention of retinal degeneration.

Photoprotective Effect of the Hydroalcoholic Extract from Red and Black Peruvian Varieties of <i>Phaseolus vulgaris</i> L.

Introduction: Ultraviolet radiation can be harmful to the skin and can create serious problems when a protective substance or equipment is not used regularly, for this reason the present study set out to evaluate the photoprotective effect of the hydroalcoholic extracts of the integument of the red and black varieties of pop beans (Phaseolus vulgaris). Materials and Method: The extracts were obtained by macerating the tegument of the two varieties of pop beans, black and red, in an ethanol/water (80:20) solution. The thin-layer chromatographic method was used to observe anti-tyrosinase activity, using the 0.05% kojic acid standard as a positive control. The photoprotective effect was evaluated in female mice of seven-week-old, Mus musculus Balb/c, with shaved back and exposed to UV-C radiation for 30 minutes once a day for thirty days to induce photo-damage in the skin. The treatments consisted in the application of extracts at 2% and 5% W/V in gel on the shaved area. Only the gel formulation, sunscreen or no treatment at all was used for the control group. Acute photodamage was quantified using the Draize scale, measuring the degree of erythema and edema; and the degree of photoaging using the Glogau scale at 7 days and 30 days. Results: It was found that the ethanolic extracts of the integument of both varieties of Phaseolus vulgaris, red and black, are practically non-toxic in mice by oral and dermal routes at a limit dose of 5000 mg/kg. The anti-tyrosinase effect at a qualitative level, evaluated by thin layer chromatography, showed the black variety were more active than the red one and both can be compared to the activity of the kojic acid. The two extracts of the two varieties showed photoprotective effect, however the extracts in 5% gel to a greater degree. Conclusions: It was concluded that the hydroalcoholic extract of the pop black beans tegument at 5% in gel has photoprotective effect.

Nanoencapsulation of Cyanidin-3- O-glucoside Enhances Protection Against UVB-Induced Epidermal Damage through Regulation of p53-Mediated Apoptosis in Mice.

Excess ultraviolet (UV) radiation causes numerous forms of skin damage. The aim of the present study was to assess and compare the photoprotective effects of cyanidin-3- O-glucoside (C3G) alone and encapsulated in chitosan nanoparticles (Nano-C3G) in a UVB-induced acute photodamage mouse model. Nano-C3G was developed from chitosan and sodium tripolyphosphate (TPP) by ionic gelation. The particle size, zeta potential, entrapment efficiency, drug loading, and in vitro release in 6 days were determined. Kunming (KM) mice were treated with Nano-C3G (125, 250, 500 μM) or C3G (500 μM) after part of the dorsal skin area was dehaired and then exposed to 2 J/cm2 of UVB. The nanocapsules were successfully produced and had a uniform and complete spherical shape without agglomeration. The size, zeta potential, entrapment efficiency, and drug loading of Nano-C3G was 288 nm, +30 mV, 44.90%, and 4.30%, respectively. C3G in the nanocapsules was released quite rapidly, and the release rate slowed down at higher pH. The animal experiment demonstrated that Nano-C3G could effectively reduce the UVB-induced lipid peroxidation, malondialdehyde, and 8-hydroxy-2'-deoxyguanosine contents; downregulate p53, Bcl-2-associated X (Bax), and caspase-3 and -9 expression; and balance the B-cell lymphoma-2/leukemia-2 ratio. Moreover, Nano-C3G (125, 250, 500 μM) improved the visual appearance, skin moisture, histologic appearance, and apoptotic index (based on TUNEL staining) under UVB exposure. In conclusion, these results suggest that Nano-C3G can reduce UVB-induced epidermal damage through the p53-mediated apoptosis signaling pathway. Moreover, Nano-C3G was more efficient than C3G at the same concentration (500 μM).

Topical Bixin Confers NRF2-Dependent Protection Against Photodamage and Hair Graying in Mouse Skin.

Environmental exposure to solar ultraviolet (UV) radiation causes acute photodamage, premature aging, and skin cancer, attributable to UV-induced genotoxic, oxidative, and inflammatory stress. The transcription factor NRF2 [nuclear factor erythroid 2 (E2)-related factor 2] is the master regulator of the cellular antioxidant response protecting skin against various environmental stressors including UV radiation and electrophilic pollutants. NRF2 in epidermal keratinocytes can be activated using natural chemopreventive compounds such as the apocarotenoid bixin, an FDA-approved food additive and cosmetic ingredient from the seeds of the achiote tree (Bixa orellana). Here, we tested the feasibility of topical use of bixin for NRF2-dependent skin photoprotection in two genetically modified mouse models [SKH1 and C57BL/6J (Nrf2+/+ versus Nrf2-/-)]. First, we observed that a bixin formulation optimized for topical NRF2 activation suppresses acute UV-induced photodamage in Nrf2+/+ but not Nrf2-/- SKH1 mice, a photoprotective effect indicated by reduced epidermal hyperproliferation and oxidative DNA damage. Secondly, it was demonstrated that topical bixin suppresses PUVA (psoralen + UVA)-induced hair graying in Nrf2+/+ but not Nrf2-/- C57BL/6J mice. Collectively, this research provides the first in vivo evidence that topical application of bixin can protect against UV-induced photodamage and PUVA-induced loss of hair pigmentation through NRF2 activation. Topical NRF2 activation using bixin may represent a novel strategy for human skin photoprotection, potentially complementing conventional sunscreen-based approaches.

Corrigendum to "Protective Effects of Soy Oligopeptides in Ultraviolet B-Induced Acute Photodamage of Human Skin".

[This corrects the article DOI: 10.1155/2016/5846865.].

A double blind, randomized, comparative study of a facial serum containing 15% L-ascorbic acid, 1% alpha-tocopherol and 0.5% ferulic acid protecting against acute photodamage in Brazilian patients

A double blind, randomized, comparative study of a facial serum containing 15% L-ascorbic acid, 1% alpha-tocopherol and 0.5% ferulic acid protecting against acute photodamage in Brazilian patients

Protective Effect of Curcumin Against Acute Ultraviolet B Irradiation-induced Photo-damage.

Ultraviolet B (UVB) irradiation is one of the most dangerous insults for skin and causes sunburn, erythema, photoaging and photocarcinogenesis. Curcumin (diferuloylmethane), a yellow spice derived from dried rhizomes of Curcuma longa, has been shown to possess significant anti-inflammatory, antioxidant, anticarcinogenic, antimutagenic, anticoagulant and anti-infective effects. However, the protective effects of curcumin against acute photo-damage are poorly understood. In this study, we investigated the photoprotective effects of curcumin against UVB-induced acute photo-damage in hairless mice and immortalized human keratinocytes (HaCaT). Topical application of curcumin significantly inhibited acute UVB (540 mJ cm-2 , for 3 successive days)-induced inflammatory cells, collagen accrementition derangement and lipid peroxidation, and effectively induced NF-E2-related factor 2 (Nrf2) nuclear accumulation in uncovered (Uncv) hairless mice skin. Treatment of HaCaT cells with curcumin significantly attenuated acute UVB (300 mJ cm-2 )-induced lactate dehydrogenase release, intracellular reactive oxygen species production and DNA damage, activated the expression of the phase II detoxifying enzymes and promoted DNA repair activity. The photoprotective effect provided by curcumin was potential associated with modulation of Nrf2-dependent antioxidant response. Our study suggested that curcumin is a potential agent for preventing and/or treating UV radiation-induced acute inflammation and photoaging.

Telomere shortening in cultured human dermal fibroblasts is associated with acute photodamage induced by UVA irradiation

IntroductionPhotoaging is the superposition of chronic ultraviolet (UV)-induced damage on intrinsic aging. Telomere length is a molecular marker of cell aging, and genomic instability due to telomere shortening has been linked to several aging-related diseases.AimTo explore the effects of different doses of ultraviolet A (UVA) on the length of telomeres in human skin fibroblasts and partly reveal the mechanism of skin photoaging initiated by UVA irradiation.Material and methodsPrimary cultured human skin fibroblasts were irradiated with different doses of UVA light. Cell viability, cell cycle phase, β-galactosidase, and the length of telomeres were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, cytochemical staining, and real-time polymerase chain reactions, respectively.ResultsAfter UVA irradiation, inhibited proliferation, S phase accumulation and increased expression of senescence-associated β-galactosidase were observed in cultured fibroblasts. Moreover, the length of telomeres in UVA-treated cells was shortened in a dose-dependent manner as compared to controls (p < 0.05).ConclusionsThese results suggest that telomere length in human dermal fibroblasts can be shortened by a single high dosage of UVA radiation, and that acute photodamage might contribute to early photoaging in human skin via rapid telomere shortening. This study potentially provides the basis for better understanding of the molecular mechanism of photoaging.

Animal Models of Acute Photodamage: Comparisons of Anatomic, Cellular and Molecular Responses in C57BL/6J, SKH1 and Balb/c Mice

Human cutaneous photodamage is a major medical problem that includes premature aging and fragility of the skin. Nonxenografted animal models have not been comparatively evaluated for how well they resemble the changes seen in human skin. Here, we sought to identify a suitable mouse model that recapitulates key anatomic, cellular and molecular responses observed in human skin during acute UV exposure. Adult females from three strains of mice, C57BL/6J, SKH1 and Balb/c were exposed to UVB and then evaluated 3 or 20 h after the last irradiation. Skin from UVB-exposed C57BL/6J mice showed features resembling human photodamage, including epidermal thickening, infiltration of the dermis with inflammatory cells, induction of tumor necrosis factor-α (TNF-α) mRNA, accumulation of glycosaminoglycans, particularly hyaluronan in the epidermis and loss of collagen. Hairless SKH1 mouse skin responded similarly, but without any induction of TNF-α mRNA or chondroitin sulfate. Irradiated Balb/c mice were the least similar to humans. Our results in C57BL/6J mice and to a lesser extent in SKH1 mice, show cutaneous responses to a course of UVB-irradiation that mirror those seen in human skin. Proper choice of model is critical for investigating cellular and molecular mechanisms of photodamage and photoaging.

Proteome analysis of ultraviolet-B-induced protein expression in vitro human dermal fibroblasts

Ultraviolet-B (UVB) radiation can result in acute photodamage, photoaging and skin cancer through the induction of reactive oxygen species, DNA damage, activation of signaling pathways, and regulation of gene expression. In this study, we investigated UVB-induced alterations in protein expression in human dermal fibroblasts. Skin fibroblasts were irradiated with 100 mJ/cm² UVB, and cell viability was monitored by the 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-diphenytetrazoliumromide assay. Two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization time of flight mass spectroscopy were used to identify differentially expressed proteins. The mRNA and levels of identified proteins were detected using a quantitative real-time polymerase chain reaction assay and Western blot. UVB decreased the viability of skin fibroblasts. In UVB-treated cells, eighteen differentially expressed proteins were identified. Among these proteins, the amounts of receptor-interacting protein (RIP) and vimentin were significantly up-regulated. However, their mRNA levels decreased and remained relatively stable, respectively. The differential expression of RIP and vimentin was validated in UVB-irradiated fibroblasts. RIP may promote cell injury, and vimentin may contribute to the resistance of cells to UVB-induced damage.