Thyroid hormone-clearing type 3 deiodinase is located in spermatogonia, where it may serve as a critical modulator of the thyroid hormone exposure of the male germ line and its epigenetic information, with implications for neurodevelopmental and endocrine disorders in subsequent generations.
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Spermatogonial Dio3 as a potential germ line sensor for thyroid hormone-driven epigenetic inheritance †.
Biol Reprod
September 2021
Center for Molecular Medicine, Maine Medical Center Research Institute, Maine Health, Scarborough, ME, USA.
Thyroid hormone-clearing type 3 deiodinase is located in spermatogonia, where it may serve as a critical modulator of the thyroid hormone exposure of the male germ line and its epigenetic information, with implications for neurodevelopmental and endocrine disorders in subsequent generations.
View Article and Find Full Text PDFSpermatogonial Type 3 Deiodinase Regulates Thyroid Hormone Target Genes in Developing Testicular Somatic Cells.
Endocrinology
December 2019
Center for Molecular Medicine, Maine Medical Center Research Institute, Maine Medical Center, Scarborough, Maine.
Premature overexposure to thyroid hormone causes profound effects on testis growth, spermatogenesis, and male fertility. We used genetic mouse models of type 3 deiodinase (DIO3) deficiency to determine the genetic programs affected by premature thyroid hormone action and to define the role of DIO3 in regulating thyroid hormone economy in testicular cells. Gene expression profiling in the neonatal testis of DIO3-deficient mice identified 5699 differentially expressed genes.
View Article and Find Full Text PDFGonadotrophin-mediated miRNA expression in testis at onset of puberty in rhesus monkey: predictions on regulation of thyroid hormone activity and DLK1-DIO3 locus.
Mol Hum Reprod
March 2019
Department of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh School of Medicine and Magee-Womens Research Institute, 204 Craft Avenue, Pittsburgh, PA, USA.
Molecular mechanisms responsible for the initiation of primate spermatogenesis remain poorly characterized. Previously, 48 h stimulation of the testes of three juvenile rhesus monkeys with pulsatile LH and FSH resulted in down-regulation of a cohort of genes recognized to favor spermatogonia stem cell renewal. This change in genetic landscape occurred in concert with amplification of Sertoli cell proliferation and the commitment of undifferentiated spermatogonia to differentiate.
View Article and Find Full Text PDFDifferential genomic imprinting and expression of imprinted microRNAs in testes-derived male germ-line stem cells in mouse.
PLoS One
December 2011
Department of Animal Biotechnology, Bio-Organ Research Center, Konkuk University, Hwayang-dong, Gwangjin-gu, Seoul, South Korea.
Background: Testis-derived male germ-line stem (GS) cells, the in vitro counterpart of spermatogonial stem cells (SSC), can acquire multipotency under appropriate culture conditions to become multipotent adult germ-line stem (maGS) cells, which upon testicular transplantation, produce teratoma instead of initiating spermatogenesis. Consequently, a molecular marker that can distinguish GS cells from maGS cells would be of potential value in both clinical and experimental research settings.
Methods And Findings: Using mouse as a model system, here we show that, similar to sperm, expression of imprinted and paternally expressed miRNAs (miR-296-3p, miR-296-5p, miR-483) were consistently higher (P<0.
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