Accumulated HSV1-TK Proteins Interfere with Spermatogenesis through a Disruption of the Integrity of Sertoli-Germ Cell Junctions

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  • CAI Li-Yi
    Department of Reproductive Medicine, The Affiliated Wuxi Hospital for Maternal and Children Health Care of Nanjing Medical University, Jiangsu Province 214002, China Institute of Reproduction and Endocrinology, Meiji University, Kanagawa 214-8571, Japan Division of Life Science, Graduate School of Agriculture, Meiji University, Kanagawa 214-8571, Japan Department of Reproductive Medicine, The Affiliated Wuxi Hospital for Maternal and Children Health Care of Nanjing Medical University, Jiangsu Province 214002, China Institute of Reproduction and Endocrinology, Meiji University, Kanagawa 214-8571, Japan Division of Life Science, Graduate School of Agriculture, Meiji University, Kanagawa 214-8571, Japan
  • KATO Takako
    Institute of Reproduction and Endocrinology, Meiji University, Kanagawa 214-8571, Japan Institute of Reproduction and Endocrinology, Meiji University, Kanagawa 214-8571, Japan
  • CHEN Mo
    Division of Life Science, Graduate School of Agriculture, Meiji University, Kanagawa 214-8571, Japan Division of Life Science, Graduate School of Agriculture, Meiji University, Kanagawa 214-8571, Japan
  • WANG HongHua
    Department of Reproductive Medicine, The Affiliated Wuxi Hospital for Maternal and Children Health Care of Nanjing Medical University, Jiangsu Province 214002, China Department of Reproductive Medicine, The Affiliated Wuxi Hospital for Maternal and Children Health Care of Nanjing Medical University, Jiangsu Province 214002, China
  • SEKINE Ei-ichiro
    Laboratory of Molecular Biology and Gene Regulation, Department of Life Science, Meiji University, Kanagawa 214-8571, Japan Laboratory of Molecular Biology and Gene Regulation, Department of Life Science, Meiji University, Kanagawa 214-8571, Japan
  • IZUMI Shun-ichiro
    Department of Obstetrics and Gynecology, Tokai University School of Medicine, Kanagawa 259-1193, Japan <i>Department of Obstetrics and Gynecology, Tokai University School of Medicine, Kanagawa 259-1193, Japan</i>
  • KATO Yukio
    Institute of Reproduction and Endocrinology, Meiji University, Kanagawa 214-8571, Japan Division of Life Science, Graduate School of Agriculture, Meiji University, Kanagawa 214-8571, Japan Laboratory of Molecular Biology and Gene Regulation, Department of Life Science, Meiji University, Kanagawa 214-8571, Japan Institute of Reproduction and Endocrinology, Meiji University, Kanagawa 214-8571, Japan Division of Life Science, Graduate School of Agriculture, Meiji University, Kanagawa 214-8571, Japan Laboratory of Molecular Biology and Gene Regulation, Department of Life Science, Meiji University, Kanagawa 214-8571, Japan

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Transgenic rats show spermatid-specific ectopic expression of the reporter gene, herpes simplex virus type1 thymidine kinase (HSV1-TK), in the testes and have demonstrated male infertility. However, the disruption of spermatogenesis and the underlying molecular mechanisms in these transgenic animals have not been well clarified. In this study, light and electron microscopic observations were performed to characterize the morphological changes in the testes. To explore the molecular mechanisms of male infertility in the HSV1-TK transgenic rat, cDNA microarray and quantitative real-time PCR analyses were performed. The seminiferous tubules of 3-month-old transgenic rats showed morphological alterations including seminiferous epithelial sloughing, vacuolization, and degeneration of spermatogenic cells, suggesting a failure of Sertoli-germ cell interaction. Components of the epididymal lumen from transgenic rats included abnormal spermatozoa, degenerating round spermatids and abnormal elongated spermatids indicating an appearance of direct impairment of spermiogenesis. cDNA microarray and real-time PCRanalyses revealed significant changes (P<0.05) in the gene expression level in six genes, testin, versican, mamdc1, fgf7, ostf1 and cnot7. Among them, testin drew most of our attention, since the testin gene is a sensitive marker for disruption of Sertoli-germ cell adhesion. Thus, our results suggest that the accumulation of HSV1-TK in the spermatids not only directly interferes with spermiogenesis but also disrupts spermatogenesis through a disruption of Sertoli-germ cell adhesions. It is important to explore the testicular actions of the HSV1-TK protein in transgenic experimental models and thereby gain clues to find an appropriate treatment for HSV-infected patients exhibiting human male infertility, as has been recently observed.

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