WCRB2014 POSTER PRESENTATIONS (1) (335 abstracts)
Androgen receptor signalling in testicular Leydig cells is essential for Leydig cell maturation and survival
Laura O’Hara 1 , Kerry McInnes 2 , Ioannis Simitsidellis 3 , Steph Morgan 1 , Laura Milne 3 , Rod Mitchell 1 & Lee Smith 3
1MRC/University of Edinburgh Centre for Reproductive Health, Edinburgh, UK; 2University of Edinburgh/British Heart Foundation Centre for Cardiovascular Science, Edinburgh, UK; 3University of Edinburgh, Edinburgh, UK.
Androgen receptor (AR) is expressed by testicular somatic cells including steroidogenic Leydig cells (LC). Its role in LC is ill defined, with hypotheses based on evidence from total androgen receptor knockout models implying that LC AR is responsible for final LC number, regulation of steroidogenic enzyme expression and LC maturation.
To better define the role of AR in LC, we generated a mouse line with a LC specific ablation of AR (LCARKO) using the Cre/lox system.
AR is ablated from 75% of LC in the LCARKO. Total LC number does not differ between LCARKO and controls. Despite reaching normal adult numbers, LC lacking AR fail to mature, as demonstrated by the significant reduction in adult LC-specific transcripts. Despite the failure of maturation, LCARKO mice have normal intratesticular testosterone levels at d80. Testicular histology is normal until d80 when focal degeneration of the seminiferous epithelium is noted, which becomes progressively worse with ageing. Testes at d180 were examined for evidence of apoptosis. None was noted in controls, however, age-matched LCARKO testes demonstrated interstital apoptosis not seen at earlier ages. Apoptosis was also noted in biopsies of post-pubertal human males with complete androgen insensitivity syndrome (CAIS).
Maturation of LC and their survival with ageing is dependent on autocrine AR signalling, but achievement of final LC number requires AR signalling in another cell type. Apoptosis of LC occurs in both LCARKO mice and CAIS humans, suggesting the underlying cause is common to both. The mechanisms of these observations are under investigation.
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ISSN 2052-1472 (online)
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