Browsing by Subject "Thyroid hormone"

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    Effects of thyroid hormones on Leydig cells in the postnatal testis
    (Murcia : F. Hernández, 2004) Mendis-Handagama, S.M.L.C.; Ariyaratne,H.B.S.
    Thyroid hormones (TH) stimulate oxidative metabolism in many tissues in the body, but testis is not one of them. Therefore, in this sense, testis is not considered as a target organ for TH. However, recent findings clearly show that TH have significant functions on the testis in general, and Leydig cells in particular; this begins from the onset of their differentiation through aging. Some of these functions include triggering the Leydig stem cells to differentiate, producing increased numbers of Leydig cells during differentiation by causing proliferation of Leydig stem cells and progenitors, stimulation of the Leydig cell steroidogenic function and cellular maintenance. The mechanism of action of TH on Leydig cell differentiation is still not clear and needs to be determined in future studies. However, some information on the mechanisms of TH action on Leydig cell steroidogenesis is available. TH acutely stimulate testosterone production by the Leydig cells in vitro via stimulating the production of steroidogenic acute regulatory protein (StAR) and StAR mRNA in Leydig cells; StAR is associated with intracellular trafficking of cholesterol into the mitochondria during steroid hormone synthesis. However, the presence and/or the types of TH receptors in Leydig cells and other cell types of the Leydig cell lineage is still to be resolved. Additionally, it has been shown that thyrotropin-releasing hormone (TRH), TRH receptor and TRH mRNA in the testis in many mammalian species are seen exclusively in Leydig cells. Although the significance of the latter observations are yet to be determined, these findings prompt whether hypothalamo-pituitary-thyroid axis and hypothalamopituitary- testis axis are short-looped through Leydig cells.
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    Thyroid hormone and anti-Mullerian hormone (AMH) on Leydig cell differentiation: studies using C57BL/6 mice and AMH over expressing mice
    (F. Hernandez y JuanF. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología., 2012) Ariyaratne, H.B.S.; Mendis-Handagama, S.M.L.C.
    Although the thyroid hormone has stimulatory effects and anti-Mullerian hormone (AMH) has inhibitory effects on prepubertal Leydig cell (LC) differentiation, it is important to find out whether the stimulatory effect of thyroid hormone could overcome the inhibitory effect of AMH on postnatal LC differentiation. Therefore, the objective of the present study was to use the anti-Mullerian hormone overexpressing mouse (AMH++) model to understand the simultaneous effects of AMH and thyroid hormone on postnatal LC differentiation, proliferation, maturation and function and to test whether the inhibitory effect of AMH could be overcome by the stimulatory effect of the thyroid hormone. Four age groups (7, 21, 40, 90 days) of control (C57BL/6; C) and AMH++ were used. Mice received either saline or triiodothyronine (T3) SC injections daily from birth to 21days. The four experimental groups were C, C+T3, AMH++ and AMH+T3. Body and testis weights of both C+T3 and AMH+T3 mice were significantly reduced at days 21, 40 and 90, compared to their age-matched saline-treated mice (C and AMH++). BrdU studies revealed the absence of LC proliferation in AMH++ mice at day7, however, same-aged mice of C+T3 and AMH+T3 mice showed increased LC proliferation; the rate was highest in C+T3 at day21. C+T3 mice of day 21 had more LC than C mice as well as AMH+T3 and AMH++ mice. At days 40 and 90, LC number/testis in C+T3 was lower than C, however, AMH+T3 had higher LC numbers than AMH++ mice. Cellular apoptosis was not seen as the cause of reduced LC numbers. Serum testosterone was not different among groups at day 21, but significantly higher levels were seen in AMH+T3 compared to AMH++ mice at days 40 and 90. Similar pattern was seen for luteinizing hormone (LH)-stimulated testicular testosterone and androstenedione production in vitro. Findings suggest that T3-treatment for the first postnatal 21 days was able to partially counteract the inhibitory effect of AMH on prepubertal LC differentiation. Whether continuation of the T3-treatment beyond 21 days would have resulted in complete removal of this inhibition, is a question that needs to be addressed.
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    Thyroxine treatment stimulated ovarian follicular angiogenesis in immature hypothyroid rats
    (Murcia : F. Hernández, 2008) Jin-Yi Jiang; Kanako Miyabayashi; Stefania A. Nottola; Motoaki Umezu; Sandra Cecconi; Eimei Sato; Guido Macchiarelli
    Summary. The development of mature ovarian follicles is greatly dependent on healthy thecal angiogenesis. Recent experimental evidence showed that thyroxine (T4) treatment promoted ovarian follicle development in immature hypothyroid (rdw) rats. However, an involvement of thyroid hormone in ovarian follicular angiogenesis has not yet been demonstrated. By morphological and molecular approaches, the present studies demonstrated that antral follicles in untreated, T4- or equine chorionic gonadotropin (eCG)-treated rdw rats were mainly small and/or atretic, and presented a poorly developed thecal microvasculature with ultrastructural evidence of diffuse quiescent or degenerative thin capillaries. However, T4 together with eCG increased the number of large antral and mature follicles with numerous activated capillaries and ultra-structural evidence of rich and diffuse angiogenesis in the theca layer. While T4 alone significantly increased mRNA expression of vascular endothelial growth factor (VEGF) and tumor necrosis factor alpha (TNFα), it decreased that of fetal liver kinase compared with those in the untreated group. Combined treatment of T4 and eCG markedly increased mRNA abundance of not only VEGF and TNFα, but also basic fibroblast growth factor. These data suggest that T4 may promote ovarian follicular angiogenesis in rdw rats by up-regulating mRNA expression of major angiogenic factors.