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Research Seeks Infertility Cause in Transgenic Mice

Simian virus 40 large T antigen expression may disrupt gonadotropin production

FRIDAY, March 20 (HealthDay News) -- In GnRHR-TAg transgenic mice, females may be infertile due to altered gonadotropin production and secretion before they even develop pituitary tumors, according to research published online March 12 in Endocrinology.

Kyeong-Hoon Jeong, Ph.D., of Harvard Medical School in Boston, and colleagues analyzed data from transgenic mice that develop gonadotrope-derived pituitary tumors at 4 to 5 months of age. Females are infertile throughout their lives, but males are capable of reproduction until their tumors grow large.

The investigators found that female mice showed lower plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels and pituitary LHβ and FSHβ subunit protein levels. Transgenic females had underdeveloped ovaries and uteri compared to non-transgenic littermates at two months, and their ovaries remained smaller and uteri thinner at 5 months; males showed no differences in reproductive organs. The authors report that simian virus 40 large T antigen (SV40 TAg) expression may be enough to alter gonadotropin production.

"Although we have not yet identified the specific mechanisms by which SV40 TAg disrupts gonadotropin production, the repression of cellular specification of gonadotropes is unlikely, since GnRHR [gonadotropin releasing hormone receptor] expression levels, a marker specific for gonadotropes in the pituitary, was normal. We can speculate, however, that SV40 TAg may interfere, either directly or indirectly, with LHβ and FSHβ subunit gene expression and hence protein biosynthesis," the authors write.

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