Ovarian iodide uptake and triiodothyronine generation in follicular fluid

Slebodzinski, A B

doi:10.1016/j.domaniend.2005.02.029

Cited by 37 publications

(30 citation statements)

References 28 publications

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“…This is the first description of such a chain of events linking reduced availability of a trace element, i.e., iodide and physiological angiogenesis. Because the iodide symporter NIS is expressed in organs other than the thyroid (trophoblast, breast, ovaries, salivary glands, stomach, cardiomyoblasts) (4,8,20,26,35,36), it might be proposed that a similar mechanism for VEGF-A regulation by iodide exists in cell types other than thyrocytes. Whether this newly described regulatory pathway exists in other cell types or for other trace elements remains to be elucidated.…”

Section: Discussionmentioning

confidence: 98%

Iodide deficiency-induced angiogenic stimulus in the thyroid occurs via HIF- and ROS-dependent VEGF-A secretion from thyrocytes

Gérard¹,

Poncin²,

Audinot³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Vascular supply is an obvious requirement for all organs. In addition to oxygen and nutrients, blood flow also transports essential trace elements. Iodine, which is a key element in thyroid hormone synthesis, is one of them. An inverse relationship exists between the expansion of the thyroid microvasculature and the local availability of iodine. This microvascular trace element-dependent regulation is unique and contributes to keep steady the iodide delivery to the thyroid. Signals involved in this regulation, such as VEGF-A, originate from thyrocytes as early TSH-independent responses to iodide scarcity. The question raised in this paper is how thyrocytes, facing an acute drop in intracellular stores of iodine, generate angiogenic signals acting on adjacent capillaries. Using in vitro models of rat and human thyroid cells, we show for the first time that the deficit in iodine is related to the release of VEGF-A via a reactive oxygen species/hypoxia-inducible factor-1-dependent pathway.

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Section: Discussionmentioning

confidence: 98%

Iodide deficiency-induced angiogenic stimulus in the thyroid occurs via HIF- and ROS-dependent VEGF-A secretion from thyrocytes

Gérard¹,

Poncin²,

Audinot³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…Deiodinase (DIO) enzymes are essential in the activation and deactivation of thyroid hormones. Previous studies revealed that the 5′‐monodeiodinase (MD) activity was positively correlated with serum T4 but not with serum T3 levels; and the existence of the ovarian 5′‐MD system was able to generate T3 from T4, with T3 then interacting with thyroid hormone nuclear receptor (Slebodzinski, ). Our previous data also revealed that thyroxine (T4) plays important roles in follicular development in the ovaries of postnatal and immature rats (Fedail et al, ), and we therefore used T4 in the present study.…”

Section: Methodsmentioning

confidence: 99%

Bisphenol A attenuates thyroxine‐induced apoptosis in ovarian granulosa cells of pigs

Song

Wei

et al. 2019

Reprod Domestic Animals

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Contents Bisphenol A (BPA) is a chemical of high production volume that is used widely in many industries and is known as a xenooestrogen and anti‐thyroid hormone endocrine disrupter. There is little information regarding the effects of BPA in the presence of thyroid hormone on porcine granulosa cell development. Thus, the primary granulosa cells were treated with thyroxine (T4, 10 nM), BPA (10 µM) or T4 plus BPA; we subsequently evaluated the effects of T4 or BPA on 17β‐estradiol synthesis, cellular proliferation and apoptosis. Our data showed that BPA significantly increased the accumulation of 17β‐estradiol and promoted granulosa cell proliferation, whereas T4 significantly decreased 17β‐estradiol and had no effect on cellular proliferation. In addition, it was noteworthy that T4 treatment induced apoptosis in porcine granulosa cells and BPA co‐incubation attenuated T4‐induced apoptosis as shown from flow cytometric assay analysis. We hypothesized that BPA attenuates T4‐induced apoptosis by regulating 17β‐estradiol accumulation and oestrogen receptor‐mediated signalling pathways. In conclusion, our results demonstrated that T4 affected 17β‐estradiol accumulation and induced cellular apoptosis, but did not affect granulosa cell proliferation. Exposure to BPA increased 17β‐estradiol accumulation, promoted granulosa cell proliferation and attenuated T4‐induced apoptosis in porcine granulosa cells in vitro.

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“…(15) Our results show higher serum concentrations of fT4 in the group of mares treated with hCG than in the control ones. Even if fT4 concentrations declined in both the groups, they persisted at statistically higher levels (p < 0,05) for 48 hours in the treated group B, compared with the control group A.…”

Section: Discussionmentioning

confidence: 46%

Thyreotropic effect of human Chorionic Gonadotropin (hCG) in mares at estrus

Rizzo¹,

Mutinati²,

Spedicato³

et al. 2009

Immunopharmacology and Immunotoxicology

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The beta-subunits of thyroid stimulating hormone (TSH) and human chorionic gonadotropin (hCG) share a high homology, just like the ectodomains of their receptors, do. As a consequence, hCG was shown to exert a thyrotropic action in humans and hamsters. This study aimed to investigate whether hCG, used to induce ovulation, displays a thyrotropic effect in the equine species too. Forty mares at estrus were divided in two groups; 20 were intravenously treated with sterile saline solution (NaCl 0.9%) (group A); 20 were intravenously treated with 4000 I.U. of hCG (group B). All the mares were artificially inseminated 24 hours after the administration of the drugs and underwent blood collection at estrus detection (T1), 2, 6, 24 hours later (T2, T3, T4), and 3 and 6 days later (T5, T6), in order to detect serum fT3 and fT4 concentrations. fT3 concentrations gave rise to similar and constant trends in the two groups, without any statistically significant difference, whereas fT4 concentrations declined in both groups, remaining statistically higher in group B than in group A for 48 hours (p < 0.05), thus accounting for a thyrotropic effect of hCG. Pregnancy rate was 70% in group B and 40% in group A, respectively. The higher success in the outcome of pregnancy may result from the immunomodulating and steroidogenic effects of hCG and from the higher levels of thyroid hormones observed in the hCG treated group.

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Ovarian iodide uptake and triiodothyronine generation in follicular fluid

Cited by 37 publications

References 28 publications

Iodide deficiency-induced angiogenic stimulus in the thyroid occurs via HIF- and ROS-dependent VEGF-A secretion from thyrocytes

Iodide deficiency-induced angiogenic stimulus in the thyroid occurs via HIF- and ROS-dependent VEGF-A secretion from thyrocytes

Bisphenol A attenuates thyroxine‐induced apoptosis in ovarian granulosa cells of pigs

Thyreotropic effect of human Chorionic Gonadotropin (hCG) in mares at estrus

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