Abstract
Chronic UVB-exposure and declined estradiol production after menopause represent important factors leading to extrinsic and intrinsic aging, respectively. Remodeling of the extracellular matrix (ECM) plays a crucial role in both responses. Whether the dermal ECM is able to recover after cessation of UVB-irradiation in dependence of estradiol is not known, however of relevance when regarding possible treatment options. Therefore, the endogenous sex hormone production was depleted by ovariectomy in female mice. Half of the mice received estradiol substitution. Mice were UVB-irradiated for 20 weeks and afterwards kept for 10 weeks without irradiation. The collagen-, hyaluronan- and proteoglycan- (versican, biglycan, lumican) matrix, collagen cleavage products and functional skin parameters were analyzed. The intrinsic aging process was characterized by increased collagen fragmentation and accumulation of biglycan. Chronic UVB-irradiation additionally augmented the lumican, versican and hyaluronan content of the dermis. In the absence of further UVB-irradiation the degradation of collagen and accumulation of biglycan in the extrinsically aged group was perpetuated in an excessive matter. Whereas estradiol increased the proteoglycan content, it reversed the effects of the perpetuated extrinsic response on collagen degradation. Suspension of the intrinsic pathway might therefore be sufficient to antagonize UVB-evoked long-term damage to the dermal ECM.
Highlights
Chronic UVB-exposure and declined estradiol production after menopause represent important factors leading to extrinsic and intrinsic aging, respectively
Two specific questions were addressed for the first time: (i) is the UVB-induced degeneration of the extracellular matrix (ECM) reversible during a 10 week recovery period and (ii) does E2 as intrinsic factor mediate specific effects on the ECM during UVB-irradiation and during the UV-free recovery period
To address these questions mice were irradiated with UVB three times a week (1 minimal erythema dose (80 mJ/cm2) for 20 weeks and the UVB-mediated effects on the matrix were determined
Summary
Chronic UVB-exposure and declined estradiol production after menopause represent important factors leading to extrinsic and intrinsic aging, respectively. Whereas estradiol increased the proteoglycan content, it reversed the effects of the perpetuated extrinsic response on collagen degradation. Factors leading to dermal skin aging can be categorized into intrinsic and extrinsic responses. Up to date investigations interrogating the question whether the skin is able to recover from chronic UVB-irradiation are still lacking It is unknown whether or not the processes of intrinsic and extrinsic aging are interconnected and if activation of the intrinsic pathway can abrogate remodeling processes induced by extrinsic aging. Repeating damage through successive UV-irradiations is only repaired insufficiently as a result of glycylation products which cannot be degraded[7] Both accumulation of these micro-lesions and additional loss of total skin www.nature.com/scientificreports/. It was shown that acute UVB-irradiation leads to an increase of dermal HA15 whereas studies investigating chronic irradiation reported a decrease of dermal HA16,17
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