Conflict of Interest The authors declare no conflicting or competing commercial interests.
17β-estradiol protects human skin fibroblasts and keratinocytes against oxidative damage
Article first published online: 18 SEP 2012
© 2012 The Authors. Journal of the European Academy of Dermatology and Venereology © 2012 European Academy of Dermatology and Venereology
Journal of the European Academy of Dermatology and Venereology
How to Cite
Bottai, G., Mancina, R., Muratori, M., Di Gennaro, P. and Lotti, T. (2012), 17β-estradiol protects human skin fibroblasts and keratinocytes against oxidative damage. Journal of the European Academy of Dermatology and Venereology. doi: 10.1111/j.1468-3083.2012.04697.x
Funding source None.
- Article first published online: 18 SEP 2012
- Received: 27 April 2012; Accepted: 13 August 2012
Background Reactive oxygen species (ROS) cause severe damage to extracellular matrix and to molecular structure of DNA, proteins and lipids. Accumulation of these molecular changes apparently constitutes the basis of cell ageing. 17b-estradiol (E2) has a key role in skin ageing homeostasis as evidenced by the accelerated decline in skin appearance seen in the perimenopausal years. Oestrogens improve many aspects of the skin such as skin thickness, vascularization, collagen content and quality. Despite these clinical evidences, the effects of oestrogens on skin at the cellular level need further clarification.
Materials and Methods HaCaT and human fibroblasts were cultured under various conditions with E2 and H2O2; then were subjected to immunofluorescence and western blot analysis. Lipoperoxidation was investigated using BODIPY.
Results In human fibroblasts oxidative stress decreases procollagen-I synthesis, while E2 significantly increases it. Fibroblasts and HaCaT cells viability in the presence of E2 demonstrates a notably increased resistance to H2O2 effects. Furthermore E2 is able to counteract H2O2-mediated lipoperoxidation and DNA oxidative damage in skin cells.
Discussion In this study we highlight that the menopause-associated oestrogens decline is involved in reduced collagen production and that E2 could counteract the detrimental effects of oxidative stress on the dermal compartment during skin aging. Furthermore, our data show that physiological concentrations of oestrogens are able to interfere with ROS-mediated cell viability reduction and to protect human skin cells against oxidative damage to cellular membranes and nucleic acids structure.
Conclusion Our experimental data show that the presence of 17β-estradiol may protect skin cells against oxidative damage and that the dramatic lowering of oestrogen levels during menopause, could render skin more susceptible to oxidative damage.