Apoptosis-inhibitor Aven is downregulated in defective spermatogenesis and a novel estrogen target gene in mammalian testis  

Oleh:

Laurentino, Sandra ; Joao, Goncalves ; Cavaco, Jose Eduardo ; Oliveira, Pedro Fontes

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 96 no. 03 (Sep. 2011), page 745-750.
Topik: Aven; apoptosis; caspase inhibitor; 17ß-estradiol; testis; seminiferous tubules; Sertoli cells; spermatogenesis

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2011.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Objective To study the expression and localization of Aven in rat and human testis from azoospermic patients with different etiologies and its regulation by estrogens. Design Experimental study. Setting University research center and private IVF clinic. Patient(s) Six men with obstructive azoospermia, five with hypospermatogenesis, and six with Sertoli cell–only syndrome; male Wistar rats. Intervention(s) Testicular biopsies and rat seminiferous tubules (SeT) cultured in the presence or absence of 17ß-estradiol (E2). Main Outcome Measure(s) Testicular cell localization of Aven protein was analyzed by immunohistochemistry. Expression levels of Aven in testicular biopsies and cultured SeT, in the presence or absence of 17ß-estradiol, were determined by quantitative reverse transcription–polymerase chain reaction and Western blot. Result(s) Aven is expressed in Sertoli cells, spermatocytes, and spermatogonia of both rat and human testis. Aven is underexpressed in the testis of men with nonobstructive azoospermia, and its expression levels correlate with severity of spermatogenic status. Aven expression is regulated by E2 in rat SeT cultured ex vivo. Conclusion(s) The results suggest that deregulation of the expression of the apoptosis inhibitor Aven may be related to male factor infertility. Moreover, Aven is an estrogen target gene and may be involved in the mechanism of testicular apoptosis control by estrogens.

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