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Williams, M.R., Ling, S., Dawood, T., Hashimura, K., Dai, A., Li, H., Liu, J.P., Funder, J.W., Sudhir, K. and Komesaroff, P.A. (2002) Dehydroepiandrosterone Inhibits Human Vascular Smooth Muscle Cell Proliferation Independent of ARs and ERs. The Journal of Clinical Endocrinology & Metabolism, 87, 176-181. http://dx.doi.org/10.1210/jcem.87.1.8161

has been cited by the following article:

• TITLE: In-Vitro Determination of Biological and Anabolic Functions of Weak Androgen Dehydroepiandrosterone (DHEA) Using a Variety of Cell Lines

  AUTHORS: James L. Cox, Yingzi Chang, Pandurangan Ramaraj

  KEYWORDS: Dehydroepiandrosterone, Various Cell Lines, Biological Functions, Anabolic Function

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.5 No.8, August 26, 2015

  ABSTRACT: Dehydroepiandrosterone (DHEA) is a weak androgen and is shown to have anti-cancer, anti-atherogenic, anti-adipogenic and anti-inflammatory effects on mouse, rat and rabbit models. However, human clinical trials data did not support animal findings and were inconclusive. These systemic differences in biological actions between rodents and humans were attributed to the low level of DHEA in rodents. In order to further understand the differences in biological functions between rodents and humans, we resorted to an in-vitroapproach involving mouse, rat and human cell lines to assess DHEA biological and anabolic functions separately and independently without systemic influence. Results indicated that DHEA was effective on mouse and rat cell lines but not on human cell lines, as observed in in-vivo studies. In addition, our in-vitrostudy showed that DHEA was able to induce myogenesis in mouse mesenchymal cells revealing its anabolic function, even though DHEA was considered as a weak androgen. This observation lent credence to the ban on DHEA by IOC medical commission, citing DHEA as an anabolic steroid. These in-vitro experiments suggested that the differences in biological actions of DHEA between rodents and humans existed not only in-vivo at the systemic level, but also in-vitro at the cellular level and thus paving the way to study the mechanism responsible for these differences at the cellular level itself.