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Leydig cell function in mice lacking connexin43

¹ Departments of Physiology and Pharmacology, ² Obstetrics and Gynaecology, ³ Paediatrics, ⁴ Medicine, The University of Western Ontario, London, Ontario, Canada N6A 5C1 and ⁵ Children’s Health Research Institute, 800 Commissioners Road East, London, Ontario, Canada N6C 2V5

Correspondence should be addressed to G M Kidder; Email: gerald.kidder{at}schulich.uwo.ca

Connexin43 (Cx43) is the most abundantly expressed member of the connexin (gap junction protein) family and the only one so far identified in mouse Leydig cell gap junctions. Mice lacking Cx43 were used to investigate its role in testicular androgen production and regulation. Testes from term fetuses were grafted under the kidney capsules of castrated adult males. After 3 weeks, serum from host mice was analyzed for androgens. In order to test their response to stimulation, the grafted testes were incubated in vitro with varying concentrations of LH and their androgen end products analyzed. Incubation with radiolabeled progesterone was followed by high performance liquid chromatography to quantify the androgen-intermediate metabolites. Radiolabeled testosterone in the presence of NADPH was used to determine the activity of testosterone-metabolizing enzymes 17ß-hydroxysteroid dehydrogenase (17ßHSD), 5-reductase (5R), and 3-hydroxysteroid dehydrogenase (3 HSD). Serum androgen levels did not differ between hosts carrying wild-type versus null mutant grafts although Cx43-deficient testes had more 17ßHSD and 5R activity than wild-type controls. Furthermore, the genotype of grafted testes did not influence LH-stimulated androgen production in vitro. These results indicate that the steroidogenic function of Leydig cells is not compromised by the absence of Cx43, perhaps because other gap junction proteins are present. Dye transfer experiments demonstrated that Cx43-deficient Leydig cells retain intercellular coupling, indicating that Cx43 is not the only protein contributing to their gap junctions. Thus, despite their prominence in Leydig cells, Cx43 gap junctions are not essential for androgen production.

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