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Human fetal testis: second trimester proliferative and steroidogenic capacities
T J Murray1, P A Fowler, D R Abramovich
1Nutrition and Development, The Rowett Research Institute, Bucksburn, Aberdeen, Scotland AB21 9SB.
The Journal of Clinical Endocrinology and Metabolism
|January 3, 2001
Summary
Leydig cell hyperplasia during fetal development involves increasing numbers of proliferating cells and enhanced steroidogenic enzyme expression. This is critical for normal human gonad development.
Area of Science:
- Developmental Biology
- Reproductive Endocrinology
- Cell Biology
Background:
- Leydig cell hyperplasia (14-18 weeks gestation) is vital for human fetal testis development.
- Understanding spatio-temporal marker distribution is key to normal gonadogenesis.
Purpose of the Study:
- To investigate the distribution of developmental and functional markers in the human fetal testis (13-19 weeks gestation).
- To characterize Leydig cell hyperplasia and its associated molecular changes.
Main Methods:
- Immunohistochemistry for proliferating cell nuclear antigen, c-Myc, steroidogenic enzymes (3beta-HSD, P450c17), androgen receptor, Bcl-2, and Bax.
- In situ hybridization for P450c17 mRNA.
- Image analysis for cell quantification.
Main Results:
- Proliferating cells increased in the interstitium during Leydig cell hyperplasia.
- Steroidogenic enzymes (3beta-HSD, P450c17) expression increased in Leydig cells.
- Bcl-2 (anti-apoptotic) and Bax (pro-apoptotic) showed differential localization in peritubular myoid and Sertoli cells, respectively.
Conclusions:
- Human fetal Leydig cell hyperplasia is marked by increased proliferation and steroidogenic enzyme expression.
- Peritubular myoid cell survival may be facilitated by Bcl-2 positivity and Bax negativity.