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This Article Accepted manuscript (PDF) Supplementary Tables All Versions of this Article: JME-08-0107v1 42/4/291    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Abel, M. Articles by O'Shaughnessy, P. Search for Related Content PubMed PubMed Citation Articles by Abel, M. Articles by O'Shaughnessy, P.

M Abel, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom
D Baban, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom
S Lee, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom
H Charlton, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom
P O'Shaughnessy, Division of Cell Sciences, Institute of Comparative Medicine, University of Glasgow Veterinary School, Bearsden Rd., Glasgow G61 1QH Scotland, U.K, University of Glasgow, Glasgow, G61 1QH, United Kingdom

Correspondence: Peter O'Shaughnessy, Email: P.J.OShaughnessy{at}vet.gla.ac.uk

Abstract

Follicle stimulating hormone (FSH) acts through the Sertoli cell to ensure normal testicular development and function. To identify transcriptional mechanisms through which FSH acts in the testis we have treated gonadotrophin-deficient hypogonadal (hpg) mice with recombinant FSH and measured changes in testicular transcript levels using microarrays and real-time PCR 12, 24 and 72h after the start of treatment. Approximately 400 transcripts were significantly altered at each time point by FSH treatment. At 12h there was a clear increase in the levels of a number of known Sertoli cell transcripts (eg Fabp5, Lgals1, Tesc, Scara5, Aqp5). Additionally, levels of Leydig cell transcipts were also markedly increased (eg Ren1, Cyp17a1, Akr1b7, Star, Nr4a1). This was associated with a small but significant rise in testosterone at 24 and 72h. At 24h, androgen-dependent Sertoli cell transcripts were upregulated (eg Rhox5, Drd4, Spinlw1, Tubb3 and Tsx) and this trend continued up to 72h. In contrast to the somatic cells, only 5 germ cell trancripts (Dkkl1, Hdc, Oct4, Zfp541 and 1700021K02Rik) were altered by FSH within the time-course of the experiment. Analysis of canonical pathways showed that FSH induced a general decline in transcripts related to formation and regulation of tight junctions . Results show FSH acts directly and indirectly to induce rapid changes in Sertoli cell and Leydig cell transcript levels in the hpg mouse but that effects on germ cell development must occur over a longer time span.