pe me la cosa più interessante è la scoperta dell'attivazione del TGF Beta1 da parte dei radicali liberi.
Role of Reactive Oxygen Species (ROS) on Androgen-Inducible TGF-Beta1 Regulation
of Dermal Papilla Cells
H.G. Yoo, Y.J. Kang, S.R. Lee, H.K. Pyo, O.S. Kwon,
K.H. Kim, H.C. Eun, K.H. Cho
Department of Dermatology, Seoul National University,
College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital and Institute of Dermatological Science, Seoul National University, Seoul, Korea Little is known about the roles of androgen on the regulation of redox states in dermal papilla cells, a cellular process known to profoundly increase with aging. The androgen receptor (AR) has been reported to modulate TGF-Beta1/Smad signaling and to be overexpressed in androgen-dependent scalp areas of patients with androgenetic alopecia. The rat vibrissae dermal papilla cell line (DP-6) over-expressed with AR was investigated to evaluate the role of ROS on androgen-induced increase of TGF-Beta1 secretion. AR stablytransfected DP-6 cells were incubated with R1881 or dihydrotestosterone (DHT). Flow cytometry and laser scanning confocal microscopy were undertaken to measure ROS production and an ELISA assay to evaluate TGF-Beta1 secretion after androgen treatment. A TGF-Beta1 promoter activity assay was also performed whether to be influenced by pretreatment of ROS scavengers. Androgen markedly increased ROS generation and the androgen-inducible ROS augmented TGF-Beta1 secretion from dermal papilla cells. Treatment with ROS scavenger or several species of inhibitors decreased ROS production and TGF-Beta1 expression. Luciferase reporter assays showed suppression of TGF-Beta1 promoter signaling by ROS scavengers. In conclusion, our study shows for the first time that androgen-induced TGF-Beta1 accumulation in dermal papilla cells would be mediated by ROS production and prevented by antioxidants or ROS inhibitors.
Study of Cell Senescence in Cultured Primary Balding and Non-Balding
Dermal Papilla Cells
A.W. Bahta
Dermatology (QMUL), London, UK
The dermal papilla (DP) expresses androgen receptors and is known to control normal hair growth. The paradox of androgen action in human hair growth is well established but the molecular mechanisms are poorly understood. DP cells derived from frontal (balding) human scalp hair follicles (BDPC) are used to study androgenetic alopecia. Cultured BDPC are known to have a much slower rate of growth in vitro than DP from non-balding sites (NBDPC), however, the cause of this has not been reported. In this study we have investigated the growth of human BDPC and NBDPC in vitro. We observed that BDPC have a limited life span of 2–6 passages. We observed that from passage 2 onwards BDPC but not NBDPC showed a large flattened morphology characteristic of senescent fibroblasts and that once they had assumed this morphology they could no longer be passaged. We showed that these BDPC but not NBDPC of the same passage expressed senescence-associated beta-galactosidase activity at pH-6. Moreover, stress-induced premature senescence was induced with more prominent characteristic behaviour in BDPC than NBDPC after exposure to sub-cytotoxic levels of H2O2 a known inducer of oxidative stress. Finally BDPC also expressed a wide range of [b oxidative stress markers including HSP27, Super Oxide Dismutase and Catalase. These data suggest that the well documented, slower in vitro proliferative rate of BDPC is due in part to [b premature senescence. Moreover, our observation that cultured BDPC express markers of oxidative stress and their response to H2O2 suggest that oxidative stress may play a major role in male pattern hair loss. Others and we have observed that DHT is able to induce TGF-Beta1 in BDPC. TGF-Beta1 is known to induce oxidative stress[/b] and this may therefore, link androgens with oxidative stress[/b] and help explain the paradox of androgen action on hair growth.
quanto all'eucalipto ho trovato questo:
http://www.scisoc.or.th/stt/31/sec_b/paper/stt31_B0010.pdf
chi ha voglia di spulciare i riferimenti bibliografici di questo pdf?
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