The effect of hypothyroidism on Sertoli cell proliferation and differentiation and hormone levels during testicular development in the rat.

Haaster, L H van; Jong, Frank H. de; Docter, R.; Rooij, Dirk G. de

doi:10.1210/endo.131.3.1505485

Cited by 146 publications

(103 citation statements)

References 7 publications

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“…Therefore, neonatal hypothyroidism for about 3 weeks may affect FSH secretion from the pituitary gland throughout life, and an especially significant reduction of FSH levels was apparent after 7 weeks of age in rdw rats. This corresponds well with the finding of a previous report in which hypothyroidism was induced in rats approaching puberty [19,28] and suggests that thyroid hormone deficiency may seriously affect FSH secretion in male rats [30,31]. The depressed serum level of FSH may be the cause of delayed maturation of Sertoli cells in hypothyroid rats [28,32,33].…”

Section: Discussionsupporting

confidence: 92%

“…The FSH levels of rdw rats were markedly lower than those of N rats at 7 w and later. Earlier reports showed that FSH levels reduce during the immature stages in chemically induced hypothyroid rats [19,28,29], and that FSH l e v e l s i n t r a n s i e n t h y p o t h y r o i d r a t s a r e permanently reduced through even much later euthyroid periods of life [19]. The duration of the hypothyroid state resulting from transient hypothyroidism induced by PTU was almost the same as that caused by congenital hypothyroidism in rdw rats, i.e.…”

Section: Discussionmentioning

confidence: 97%

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Developmental Hormonal Profiles in rdw Rats with Congenital Hypothyroidism Accompanying Increased Testicular Size and Infertility in Adulthood

Umezu

Kagabu

Jiang

et al. 2004

Journal of Reproduction and Development

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Abstract. Congenital hypothyroid mutant male rdw rats have enlarged testes in adulthood with dwarfism accompanied by infertility. To explain how rdw rats acquire enlarged testes in adulthood, we compared age-matched normal (N) rats at various developmental stages for blood levels of hormones, thyroxine (T4), follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (T), and investigated whether T4 therapy (rdw+T4) from 3 weeks of age (w) until adulthood could induce recovery of fertility in rdw rats, as well as how rdw+T4 affected hormonal patterns. Testes weights of rdw rats were higher than those of N rats at 19 w in adulthood though it was low during development. Serum T4 values in rdw rats were markedly lower than those in N rats but steadily increased up to 19 w. The serum FSH values in rdw rats were lower than those in N rats at all ages, and neither serum LH nor T value was significantly different at any age. The testes weight of rdw+T4 rats was significantly higher than that of N rats at 13 w with recovered growth, and was higher than that of rdw rats at 19 w. When they were mated with proestrous females after 16 w, all females became pregnant and gave birth to a normal number of pups. The T4 and FSH values of rdw+T4 rats were significantly higher than those in rdw rats, but similar to those in N rats in adulthood. The results suggest that even low levels of circulating thyroid hormone (TH) in rdw rats stimulate the development of their testes, probably through Sertoli cells, resulting in the enlarged adult testes without fertility, and that a sufficient circulating TH level from the immature stage plays a pivotal role in restoring mating activity, probably through FSH-mediated action towards adulthood.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 97%

Developmental Hormonal Profiles in rdw Rats with Congenital Hypothyroidism Accompanying Increased Testicular Size and Infertility in Adulthood

Umezu

Kagabu

Jiang

et al. 2004

Journal of Reproduction and Development

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“…Several other factors have been demonstrated to regulate Sertoli cell development in the time interval under investigation here, including thyroid hormone (Cooke & Meisami 1991, Van Haaster et al 1992, activin (Boitani et al 1995, Fragale et al 2001, Buzzard et al 2003, glial cell line-derived neurotrophic factor (GDNF) (Hu et al 1999), interleukin-1 (Petersen et al 2002), and transforming growth factor (TGF) and epidermal growth factor (Petersen et al 2001). Interactions between these factors and FSH-mediated regulation of Sertoli cell function is not well understood, though two previously identified FSH regulated target genes, cyclin D2 (Buemer et al 2000) and DMRT-1 (Raymond et al 2000) are potential mediators.…”

Section: Sertoli Cell Developmentmentioning

confidence: 99%

Developmentally distinct in vivo effects of FSH on proliferation and apoptosis during testis maturation

Meachem¹,

Ruwanpura²,

Ziolkowski³

et al. 2005

Journal of Endocrinology

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The critical influence of follicle stimulating hormone (FSH) on male fertility relates both to its impact on Sertoli cell proliferation in perinatal life and to its influence on the synthesis of Sertoli cell-derived products essential for germ cell survival and function in the developing adult testis. The nature and timing of this shift of germ cells to their reliance on specific Sertoli cell-derived products are not defined. Based on existing data, it is apparent that the dominant function of FSH shifts between 9 and 18 day postpartum (dpp) during the first wave of spermatogenesis from driving Sertoli cell proliferation to support germ cells. To enable comprehensive analysis of the impact of acute in vivo FSH suppression on Sertoli and germ cell development, FSH was selectively suppressed in Sprague-Dawley rats by passive immunisation for 2 days and/or 4 days prior to testis collection at 3, 9 and 18 dpp. The 3 dpp samples displayed no measurable changes, while 4 days of FSH suppression decreased Sertoli cell proliferation and numbers in 9 dpp, but not 18 dpp, animals. In contrast, germ cell numbers were unaffected at 9 dpp but decreased at 18 dpp following FSH suppression, with a corresponding increase in germ cell apoptosis measured at 18 dpp. Sixty transcripts were measured as changed at 18 dpp in response to 4 days of FSH suppression, as assessed using Affymetrix microarrays. Some of these are known as Sertoli cell-derived FSH-responsive genes (e.g. StAR, cathepsin L, insulin-like growth factor binding protein-3), while others encode proteins involved in cell cycle and survival regulation (e.g. cyclin D1, scavenger receptor class B 1). These data demonstrate that FSH differentially affects Sertoli and germ cells in an age-dependent manner in vivo, promoting Sertoli cell mitosis at day 9, and supporting germ cell viability at day 18. This model has enabled identification of candidate genes that contribute to the FSH-mediated pathway by which Sertoli cells support germ cells.

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“…Transient neonatal hypothyroidism in rats produces unprecedented increases of 80 and 140% in adult testis weight and sperm production respectively . This increase in testis size results primarily from increased Sertoli cell proliferation during neonatal and juvenile life (van Haaster et al 1992) and consequent larger populations of adult Sertoli and germ cells (van Haaster et al 1992, Hess et al 1993. Sertoli cells express thyroid hormone receptor (TR) and its mRNA during the neonatal period ( Jannini et al 1990) and 3,3 ,5-triiodothyronine (T 3 ), the biologically active thyroid hormone, directly inhibits Sertoli cell proliferation in vitro .…”

Section: Introductionmentioning

confidence: 99%

Thyroid hormone effects on androgen receptor messenger RNA expression in rat Sertoli and peritubular cells

Arambepola

Bunick

Cooke

1998

Journal of Endocrinology

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Postnatal Sertoli cell maturation is characterized by a pronounced rise in androgen receptor (AR) expression, which increases several fold between birth and adulthood. Since both 3,3 ,5-triiodothyronine (T 3 ) and FSH regulate Sertoli cell proliferation and differentiation, we have determined the effects of T 3 and FSH on AR mRNA expression in cultured Sertoli cells from 5-day-old rats. These cultures contain 5-9% peritubular cells, which also express AR mRNA. To insure that the observed T 3 responses did not result from peritubular cells, we examined T 3 effects on AR mRNA expression in cultured 20-day-old Sertoli cells (which contain minimal peritubular contamination) and peritubular cells, and measured thyroid hormone receptor (TR) mRNA expression in both of these cell types. Sertoli cells from 5-and 20-day-old rat testes were grown in serum-free medium alone (controls) or with ovine FSH (100 ng/ml) and/or T 3 (100 n) for 4 days. Peritubular cells purified from 20-day-old rat testes were grown in serum-containing medium for 8 days. These cells were split 1:4, and grown an additional 8 days, the last 4 days in serum-free medium with or without T 3 . TR and AR mRNA levels in all cultures were determined by Northern blotting. AR mRNA levels in 5-and 20-day-old cultured Sertoli cells were significantly (P<0·05) increased by both T 3 and FSH alone. Furthermore, AR mRNA levels in Sertoli cells treated with T 3 and FSH were greater than with either alone. TR mRNA expression was detected in cultured peritubular cells, but TR mRNA levels in these cells were only approximately 30% of that seen in 20-day-old cultured Sertoli cells. In contrast to Sertoli cells, T 3 did not affect peritubular AR mRNA expression. These results indicate that T 3 is an important regulator of the postnatal Sertoli cell AR mRNA increase. The additive effects of maximally stimulatory doses of FSH and T 3 suggest these hormones work through different mechanisms to increase AR mRNA. TR mRNA expression in peritubular cells indicates these cells may be direct T 3 targets, though the function of T 3 in these cells is unknown.

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The effect of hypothyroidism on Sertoli cell proliferation and differentiation and hormone levels during testicular development in the rat.

Cited by 146 publications

References 7 publications

Developmental Hormonal Profiles in rdw Rats with Congenital Hypothyroidism Accompanying Increased Testicular Size and Infertility in Adulthood

Developmental Hormonal Profiles in rdw Rats with Congenital Hypothyroidism Accompanying Increased Testicular Size and Infertility in Adulthood

Developmentally distinct in vivo effects of FSH on proliferation and apoptosis during testis maturation

Thyroid hormone effects on androgen receptor messenger RNA expression in rat Sertoli and peritubular cells

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