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Endocrinology, doi:10.1210/en.2003-1049
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Endocrinology Vol. 145, No. 3 1453-1463
Copyright © 2004 by The Endocrine Society

Molecular Characterization of Postnatal Development of Testicular Steroidogenesis in Luteinizing Hormone Receptor Knockout Mice

Fu-ping Zhang, Tomi Pakarainen, Fei Zhu, Matti Poutanen and Ilpo Huhtaniemi

Department of Physiology, Institute of Biomedicine, University of Turku (F.P.Z., T.P., F.Z., M.P., I.H.), Fin-20520 Turku, Finland; Biomedicum Helsinki, Institute of Biomedicine/Physiology, University of Helsinki (F.P.Z.), 00014 Helsinki, Finland; and Institute of Reproductive and Developmental Biology, Imperial College London (I.H.), London, United Kingdom W12 0NN

Address all correspondence and requests for reprints to: Ilpo Huhtaniemi, M.D., Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, Du Cane Road, London, United Kingdom W12 0NN. E-mail: ilpo.huhtaniemi{at}imperial.ac.uk.

We recently demonstrated that the sexual development of LH receptor (LHR) knockout mice is normal until birth, but is totally arrested thereafter. To study further the functional defects of LHR knockout mice, the expression of selected Leydig cell-specific genes was studied in (-/-) and control (+/+) mice between birth and adulthood. Testis weights were similar at birth in both types of mice, but after about 3 wk, the (-/-) testes remained significantly lighter, weighing only 18% of (+/+) testes on d 70. Testicular testosterone (T) content on d 1 was also similar in (-/-) and (+/+) testes, but it was 97% reduced by d 70 in the former. Likewise, testicular T production in vitro was similar in neonatal (-/-) and (+/+) testes, but became undetectable in adult (-/-) testes. The mRNA expression of cytochrome P450 side-chain cleavage, 17{alpha}-hydroxylase cytochrome P450, 17ß-hydroxysteroid dehydrogenase type III, 3ß-hydroxysteroid dehydrogenase I (3ßHSDI), steroidogenic acute regulatory protein, and relaxin-like factor were similar in newborn (-/-) and (+/+) testes, but became gradually very low/undetectable in (-/-) mice. The only exception was the persistently high expression of 3ßHSDI in peritubular Leydig precursor and mesenchymal cells of the (-/-) testes at all ages. Immunohistochemistry and Western hybridization studies confirmed the above findings. In conclusion, LH action is not essential for the differentiation and function of mouse fetal Leydig cells, but, with the exception of 3ßHSDI, the expression of the key genes of endocrine function of adult Leydig cells is dependent on LH signaling.




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