Occurrence of testicular microlithiasis in androgen insensitive hypogonadal mice
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Occurrence of testicular microlithiasis in androgen insensitive hypogonadal mice Peter J O'Shaughnessy*1, Ana Monteiro1, Guido Verhoeven2, Karl De Gendt2 and Margaret H Abel3 Address: 1Institute of Comparative Medicine, Division of Cell Sciences, University of Glasgow Veterinary School, Bearsden Rd, Glasgow G61 1QH, UK, 2Laboratory for Experimental Medicine and Endocrinology, Catholic University of Leuven, B-3000 Leuven, Belgium and 3Department of Human Anatomy and Genetics, University of Oxford, South Parks Rd, Oxford OX1 3QX, UK Email: Peter J O'Shaughnessy* - [email protected]; Ana Monteiro - [email protected]; Guido Verhoeven - [email protected]; Karl De Gendt - [email protected]; Margaret H Abel - [email protected] * Corresponding author
Published: 27 August 2009 Reproductive Biology and Endocrinology 2009, 7:88
doi:10.1186/1477-7827-7-88
Received: 5 August 2009 Accepted: 27 August 2009
This article is available from: http://www.rbej.com/content/7/1/88 © 2009 O'Shaughnessy et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Testicular microliths are calcifications found within the seminiferous tubules. In humans, testicular microlithiasis (TM) has an unknown etiology but may be significantly associated with testicular germ cell tumors. Factors inducing microlith development may also, therefore, act as susceptibility factors for malignant testicular conditions. Studies to identify the mechanisms of microlith development have been hampered by the lack of suitable animal models for TM. Methods: This was an observational study of the testicular phenotype of different mouse models. The mouse models were: cryptorchid mice, mice lacking androgen receptors (ARs) on the Sertoli cells (SCARKO), mice with a ubiquitous loss of androgen ARs (ARKO), hypogonadal (hpg) mice which lack circulating gonadotrophins, and hpg mice crossed with SCARKO (hpg.SCARKO) and ARKO (hpg.ARKO) mice. Results: Microscopic TM was seen in 94% of hpg.ARKO mice (n = 16) and the mean number of microliths per testis was 81 +/- 54. Occasional small microliths were seen in 36% (n = 11) of hpg testes (mean 2 +/- 0.5 per testis) and 30% (n = 10) of hpg.SCARKO testes (mean 8 +/- 6 per testis). No microliths were seen in cryptorchid, ARKO or SCARKO mice. There was no significant effect of FSH or androgen on TM in hpg.ARKO mice. Conclusion: We have identified a mouse model of TM and show that lack of endocrine stimulation is a cause of TM. Importantly, this model will provide a means with which to identify the mechanisms of TM development and the underlying changes in protein and gene expression.
Background Testicular microlithiasis (TM) is characterised by the presence of microcalcifi
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