Mol. Hum. Reprod. Advance Access published online on September 2, 2009
Molecular Human Reproduction, doi:10.1093/molehr/gap070
Aromatase over expression transgenic murine models for aromatase inhibitor studies
State Key Laboratory of the Agro-Biotechnology, Faculty of Biological Sciences, China Agricultural University, Beijing 100193, China
* Correspondence: Dr. Xiangdong Li, State Key Laboratory of the Agro-Biotechnology, Faculty of Biological Sciences, China Agricultural University, Beijing 100094, China, Tel/ Fax: +86-10-6273 4389, E-mail: xiangdongli{at}cau.edu.cn
In recent years the emerging importance of estrogen signaling in males in addition to its major role in the female reproductive system became highlighted. Aromatase is the key enzyme for synthesis of estrogens from androgens and is responsible for controlling the androgen/estrogen ratio. Inhibition of aromatase gene expression can be achieved in different ways, and is important for the treatment of several estrogen-dependent diseases, such as breast cancer in females or gynecomastia/breast cancer in males, or for non-tumorigenic conditions like precocious puberty and the induction of ovulation. The inhibition of aromatase could also serve as a tool for studying the role of estrogens during development or adulthood. Using transgenic models, we are able to analyze in more detail the involvement of aromatase in the molecular mechanisms underlying the essential balance of the androgen/estrogen ratio. In this review we focus on male phenotype characterization in the aromatase overexpressing transgenic murine models and how these models can further serve as a tool for aromatase inhibitor research.
Key Words: androgen/estrogen ratio/aromatase inhibitors/estrogen excess/aromatase overexpression/transgenic mice
Footnote: This study has been supported by the grants from National Science Foundation of China (NFSC) grant number 30671506 and the Ministry of Science and Technology (MOST) No. 2009CB941701 (X.L.)
Submitted on December 15, 2008; resubmitted on July 4, 2009; accepted on August 14, 2009.