Journal
EXPERIMENTAL GERONTOLOGY
Volume 43, Issue 10, Pages 939-946Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2008.07.005
Keywords
Insulin-like growth factor-I (IGF-I); 17 beta-Estradiol; Growth hormone (GH); Progesterone; Dehydroepiandrosterone (DHEA); Insulin-like growth factor-I receptor (IGF-IR); Estrogen receptor alpha (ER alpha); Hormonal aging; Skin aging; Lipid synthesis; Cell proliferation; SZ95 sebocytes; Human skin fibroblasts
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Funding
- National Genome Research Network II (NGFN-2)
- Research on Skin Dryness Award
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In order to obtain greater insights into the molecular mechanisms accompanying hormonal aging the effects of growth hormone (GH), insulin-like growth factor-I (IGF-I), 17 beta-estradiol, progesterone and dehydroepiandrosterone were tested as single agents in concentrations corresponding to 20- and 60-year-old females on human SZ95 sebocytes and fibroblasts. Cell proliferation and viability were measured by 4-methylumbelliferyl heptanoate and lactate dehydrogenase microassays, respectively, whereas lipid accumulation was documented via nile red microassay and fluorescence microscopy. mRNA and protein expression were evaluated via real-time RT-PCR and Western blotting or ELISA, accordingly. Our results depict the importance of IGF-I for lipid synthesis in SZ95 sebocyte and demonstrate the lack of 17 beta-estradiol, dehydroepiandrosterone and progesterone activity on lipid synthesis and SZ95 sebocyte proliferation suggesting that the action of these hormones in vivo may be implemented through indirect pathways. Fibroblast showed to be more susceptible to 17 beta-estradiol treatment, while IGF-I could significantly stimulate fibroblast proliferation in a dose-dependent manner. Furthermore, an interplay between the 17 beta-estradiol and IGF-I signaling pathway was documented in both cell types. In conclusion, IGF-I is a key regulator of human skin aging and declining IGF-I levels with age may play a significant role in the reduction of skin surface lipids and thickness. (C) 2008 Elsevier Inc. All rights reserved.
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