Photoaging: Mechanisms and repair

Rabe, Jessica H.; Mamelak, Adam J.; McElgunn, Patrick J.S.; Morison, Warwick L.; Sauder, Daniel N.

doi:10.1016/j.jaad.2005.05.010

Cited by 527 publications

(425 citation statements)

References 212 publications

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“…Meanwhile, a series of photo-damages caused by chronic UV radiation including texture abnormalities, irregular pigmentation (such as solar keratosis, solar lentigo, and seborrheic keratosis) and even skin tumors, intertwine with the inherent influences and contribute to skin aging in the long run (Rabe et al, 2006;Fisher, 2005;Stern, 2004). However, factors that play important roles in skin aging and the aging patterns in different races or areas are largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Survey on skin aging status and related influential factors in Southeast China

Wang

Fang

Zhu

2009

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To investigate cutaneous aging patterns of residents in Hangzhou, Zhejiang, China, and their contributing factors. Methods: Eight hundred and forty-eight Hangzhou residents received the survey between March 2004 and September 2004. Results: Facial wrinkling first occurred at 21 years of age and skin elasticity began to lose at 22 years of age. In middle-aged and old people, facial wrinkling and looseness escalated with the increase of ultraviolet (UV)-exposure time, indicating the accelerating effect of a higher accumulative dose of UV radiation on skin aging. Only Fitzpatrick types II, III and IV were found in the skin phototypes of residents in Hangzhou area, and Fitzpatrick type II seemed to be much more subject to severe wrinkling, elasticity destruction and skin tumors than types III and IV. The oily skin was more protected against wrinkling and facial looseness than dry skin. However, as to concomitant cutaneous diseases, no difference was found among different skin types. Conclusion: Age, solar-exposure time, Fitzpatrick type and skin type are the associated forces in promoting skin aging, and emotional factor seems to be another independent risk factor. The age of 49 years and 2 h/d of solar-exposure time seem to be the turning points responsible for dramatic changes of cutaneous appearance in the process of skin aging in Southeast China.

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Section: Discussionmentioning

confidence: 99%

Survey on skin aging status and related influential factors in Southeast China

Wang

Fang

Zhu

2009

J. Zhejiang Univ. Sci. B

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“…The skin can be structurally classified into several layers, including the most apical layer, the epidermis, containing large numbers of keratinocytes, and a second layer, immediately under this, the dermis, which has a high fibroblast content (1). Skin provides a major interface between the environment and the body and is constantly exposed to an array of physical and chemical stressors.…”

mentioning

confidence: 99%

Prevention of UVB Radiation-induced Epidermal Damage by Expression of Heat Shock Protein 70

Matsuda

Hoshino

Yamashita

et al. 2010

Journal of Biological Chemistry

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Irradiation with UV light, especially UVB, causes epidermal damage via the induction of apoptosis, inflammatory responses, and DNA damage. Various stressors, including UV light, induce heat shock proteins (HSPs) and the induction, particularly that of HSP70, provides cellular resistance to such stressors. The anti-inflammatory activity of HSP70, such as its inhibition of nuclear factor kappa B (NF-B), was recently revealed. These in vitro results suggest that HSP70 protects against UVB-induced epidermal damage. Here we tested this idea by using transgenic mice expressing HSP70 and cultured keratinocytes. Irradiation of wild-type mice with UVB caused epidermal damage such as induction of apoptosis, which was suppressed in transgenic mice expressing HSP70. UVB-induced apoptosis in cultured keratinocytes was suppressed by overexpression of HSP70. Irradiation of wild-type mice with UVB decreased the cutaneous level of IB-␣ (an inhibitor of NF-B) and increased the infiltration of leukocytes and levels of pro-inflammatory cytokines and chemokines in the epidermis. These inflammatory responses were suppressed in transgenic mice expressing HSP70. In vitro, the overexpression of HSP70 suppressed the expression of pro-inflammatory cytokines and chemokines and increased the level of IB-␣ in keratinocytes irradiated with UVB. UVB induced an increase in cutaneous levels of cyclobutane pyrimidine dimers and 8-hydroxy-2-deoxyguanosine, both of which were suppressed in transgenic mice expressing HSP70. This study provides genetic evidence that HSP70 protects the epidermis from UVB-induced radiation damage. The findings here also suggest that the protective action of HSP70 is mediated by anti-apoptotic, anti-inflammatory, and anti-DNA damage effects.The skin can be structurally classified into several layers, including the most apical layer, the epidermis, containing large numbers of keratinocytes, and a second layer, immediately under this, the dermis, which has a high fibroblast content (1). Skin provides a major interface between the environment and the body and is constantly exposed to an array of physical and chemical stressors. Therefore, in addition to intrinsic causes, harmful exogenous causes are involved in the process of skin damage. Among exogenous harmful agents, UV irradiation is the most relevant to skin damage (photo-damage). UV light can be separated, based on wavelength, into three categories: UVA (320 -400 nm), UVB (290 -320 nm), and UVC (100 -290 nm). Of these, the celldamaging effect of UVA is relatively weak, whereas most UVC is absorbed by the ozone layer (2). Thus, UVB seems to play the central role in photo-damage, such as clinical sunburn, hyperpigmentation, erythema, plaque-like thickening, loss of skin tone, deep furrowing, and fine wrinkle formation, all of which constitute both clinical and cosmetic problems. Furthermore, UVB irradiation induces the development of skin cancer (photo-carcinogenesis) (3). UVB-induced photodamage and photo-carcinogenesis both involve epidermal damage (such as induction...

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“…The skin can structurally be divided into several layers including the most apical layer, the epidermis, consisting of keratinocytes (1). In addition to changes with aging, the skin is damaged by various environmental stressors, especially by solar ultraviolet irradiation (photo-aging).…”

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confidence: 99%

Suppression of Melanin Production by Expression of HSP70

Hoshino

Matsuda

Yamashita

et al. 2010

Journal of Biological Chemistry

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Skin hyperpigmentation disorders due to abnormal melanin production induced by ultraviolet (UV) irradiation are both a clinical and cosmetic problem. UV irradiation stimulates melanin production in melanocytes by increasing intracellular cAMP. Expression of heat shock proteins (HSPs), especially HSP70, is induced by various stressors, including UV irradiation, to provide cellular resistance to such stressors. In this study we examined the effect of expression of HSP70 on melanin production both in vitro and in vivo. 3-Isobutyl-1-methylxanthine (IBMX), a cAMP-elevating agent, stimulated melanin production in cultured mouse melanoma cells, and this stimulation was suppressed in cells overexpressing HSP70. IBMX-dependent transcriptional activation of the tyrosinase gene was also suppressed in HSP70-overexpressing cells. Expression of microphthalmia-associated transcription factor (MITF), which positively regulates transcription of the tyrosinase gene, was up-regulated by IBMX; however, this up-regulation was not suppressed in HSP70-overexpressing cells. On the other hand, immunoprecipitation and immunostaining analyses revealed a physical interaction between and co-localization of MITF and HSP70, respectively. Furthermore, the transcription of tyrosinase gene in nuclear extract was inhibited by HSP70. In vivo, UV irradiation of wild-type mice increased the amount of melanin in the basal layer of the epidermis, and this increase was suppressed in transgenic mice expressing HSP70. This study provides the first evidence of an inhibitory effect of HSP70 on melanin production both in vitro and in vivo. This effect seems to be mediated by modulation of MITF activity through a direct interaction between HSP70 and MITF.

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Photoaging: Mechanisms and repair

Cited by 527 publications

References 212 publications

Survey on skin aging status and related influential factors in Southeast China

Survey on skin aging status and related influential factors in Southeast China

Prevention of UVB Radiation-induced Epidermal Damage by Expression of Heat Shock Protein 70

Suppression of Melanin Production by Expression of HSP70

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