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BOR - Papers in Press, published online ahead of print December 15, 2004.
Biol Reprod 2004, 10.1095/biolreprod.104.035915
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BIOLOGY OF REPRODUCTION 72, 1010–1019 (2005)
DOI: 10.1095/biolreprod.104.035915
© 2005 by the Society for the Study of Reproduction, Inc.

Androgen-Regulated Transcripts in the Neonatal Mouse Testis as Determined Through Microarray Analysis1

Qing Zhou, James E. Shima, Rong Nie, Patrick J. Friel, and Michael D. Griswold2,

Center for Reproductive Biology, School of Molecular Biosciences, Washington State University, Pullman, Washington 99164

Androgens are required for normal spermatogenesis in mammalian testes. These hormones directly regulate testicular somatic cells that, in turn, support germ cell differentiation. However, the identity of genes under androgen regulation in the testis are not well known. In the present study, neonatal male mice (8 days postpartum) treated by testosterone propionate (TP) were used to study androgen action in the testis as evidenced by alterations in gene expression. Mice were treated with 0.5 mg of TP or dihydrotestosterone (DHT) or vehicle (oil), and testes were harvested 4, 8, and 16 h after treatment. Global gene expression was monitored by microarray analysis. Real-time reverse transcription-polymerase chain reaction was performed to confirm the microarray results. The methodology was verified by confirming the presence of previously characterized TP-regulated genes, including Pem in Sertoli cells and Cyp17a1 in Leydig cells. No significant differences in gene expression were found between TP- and DHT-treated samples. Microarray analysis identified 141, 119, and 109 up-regulated genes at 4, 8 and 16 h after TP treatment, respectively, and 83, 99, and 111 down-regulated genes at the same corresponding time points. The androgen regulation of the selected gene was verified further using testes from flutamide-treated adult mice and isolated Sertoli cells in culture. The data generated in the present study may serve as a foundation for hypothesis-driven research and provide insights regarding gene networks and pathways under androgen control in the testis.

1 Supported by grants to M.G. from the HD10808 and U54 HD42454 from NICHD and a postdoctoral fellowship from the Lalor Foundation to Q.Z.

2 Correspondence: Michael D. Griswold, 531 Fulmer Hall, School of Molecular Biosciences, Washington State University, Pullman, WA 99164-4660. FAX: 509 335 9688; mgriswold{at}wsu.edu




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