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Submitted on August 13, 2003
Accepted on November 19, 2003
1 Department of Physiology (F.P.Z., T.P., F.Z., M.P., I.H), Institute of Biomedicine, University of Turku, Kiinamynllynkatu 10, Fin-20520 Turku; Biomedicum Helsinki, Institute of Biomedicine/Physiology (F.P.Z), University of Helsinki, 00014, Helsinki, Finland and Institute of reproductive and Developmental Biology (IRDB)(I.H), Imperial College London, Du Cane Road, London W12 0NN, U.K.
* To whom correspondence should be addressed. E-mail: ilpo.huhtaniemi{at}imperial.ac.uk.
We recently demonstrated that the sexual development of LH receptor (R) knockout (LuRKO) mice is normal until birth but totally arrested thereafter. To study further the functional defects of LuRKO 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 weeks, the (-/-) testes remained significantly lighter, weighing only 18% of (+/+) testes on day 70. Testicular testosterone (T) content of day 1 was also similar in (-/-) and (+/+) testes, but it was 97% reduced by day 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 (P450scc), 17
-hydroxylase cytochrome P450 (P450-17OH), 17
-hydroxysteroid dehydrogenase type III (17HSDIII), 3-hydroxysteroid dehydrogenase I (3HSDI), steroidogenic acute regulatory protein (StAR) and relaxin-like factor (RLF) were similar in newborn (-/-) and (+/+) testes, but became gradually very low/undetectable in (-/-) mice. The only exception was the persistently high expression of 3HSDI 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 3HSDI, the expression of the key genes of the endocrine function of adult Leydig cells is dependent on LH signaling.
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