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

Gérard, A; Poncin, Sylvie; Audinot, Jean‐Nicolas; Denef, Jean‐François; Colin, Idesbald

doi:10.1152/ajpendo.90876.2008

Cited by 29 publications

(34 citation statements)

References 44 publications

(43 reference statements)

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“…On the other hand, five subjects (14.7%) among them were diagnosed as having HID. The incidence of HID is surprisingly low in view of the extremely low iodine intake but may actually be in line with other data from population studies [9][10][11][12][13][14] or may reflect difficulty in recognizing hypothyroid state in these patients or may be due to thyroid adaptive processes [15][16][17][18]. Possibly SMID patients, the targets of this study, might be at risk of developing disorders with a poor response of TSH that renders their hypothyroidism difficult to diagnose.…”

Section: Stagesupporting

confidence: 84%

“…Some experimental reports document that early thyroid adaptation develops after short-term (about one month) iodine deficiency, e.g. angiogenesis in the thyroid gland to increase iodine absorption without TSH stimulation, or tissue-selective acceleration of deiodinase activity resulting in T4 to T3 conversion [15][16][17][18]. Therefore, modest increase TSH, high normal or increased T3, and low normal or decreased T4 might be detected in iodine deficient state [19].…”

Section: Stagementioning

confidence: 99%

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Investigation of iodine deficient state and iodine supplementation in patients with severe motor and intellectual disabilities on long-term total enteral nutrition

et al. 2012

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IODINE is an essential trace element for synthesis of thyroid hormones and thyroxine (T4) is also essential for brain development. Iodine deficiency (ID) might cause hypothyroidism resulting in severe developmental delay in infants and stillbirth in pregnant women [1,2]. Patients on long-term total enteral nutrition (TEN) are at risk of ID because of the low iodine content of EN formulae (Table 1) [3][4][5]. We measured urinary iodine concentration (UIC) in patients with severe motor and intellectual disabilities (SMID) receiving long-term TEN. We also provided iodine supplementation (IS) for ID cases in the form of powdered kelp and monitored their thyroid function, UIC, biochemical parameters and vital signs. SubjectsWe enrolled 35 SMID (Male 24, Female 11, Investigation of iodine deficient state and iodine supplementation in patients with severe motor and intellectual disabilities on long-term total enteral nutrition Abstract. Iodine concentrations of enteral nutrition (EN) formulae available in Japan are very low and long-term total EN (TEN) might result in hypothyroidism due to iodine deficiency (HID). Our aim of this study was to determine the degree of iodine deficiency (ID) and need for iodine supplementation (IS) in patients with severe motor and intellectual disabilities (SMID) on long-term TEN. Thyroid function including urinary iodine concentration (UIC) was monitored, and powdered kelp was provided as a source of iodine supplement. Thirty-five SMID on TEN participated in our study. UIC less than 100 μg /L, representing ID, were detected in 97 % of them. Their TSH ranged from 0.5 to 90 μIU/mL. IS using powdered kelp raised their UIC to the normal range. Thyroid function also recovered in the five hypothyroidism cases, which were diagnosed as HID, was also detected. In Japan, there must be many cases with ID associated with long term TEN. We also discuss the regulation of thyroid function in the iodine deficient state.

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Section: Stagesupporting

confidence: 84%

Section: Stagementioning

confidence: 99%

Investigation of iodine deficient state and iodine supplementation in patients with severe motor and intellectual disabilities on long-term total enteral nutrition

et al. 2012

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“…Oxidative stress resulting from overproduction of ROS is an important intermediary step in the pathogenesis of preeclampsia and in human trophoblast differentiation [29]. Previous studies have shown that iodine deprivation induce VEGF expression through HIF-1α activation mediated by increasing ROS in thyroid cells [10]. In this study, iodine deprivation increases ROS and Snail mRNA expressions, although HIF-1α mRNA expression does not change.…”

Section: Discussionmentioning

confidence: 47%

“…Peroxisome proliferator-activated receptor gamma (PPARgamma) induces trophoblast differentiation through GCM-1 that promotes differentiation of underlying cytotrophoblast cells into the outer syncytiotrophoblasts layer [6,7]. In the thyroid gland, intracellular iodine concentration plays an important role in redox balance by modulating hydrogen peroxide generation [8,9] and thyroid iodine deficiency induced intracellular production of reactive oxygen species (ROS) that stabilizes HIF-1α protein and then the expression and secretion of vascular epithelial growth factor (VEGF) for novel blood vessels [10]. It has been proposed that in thyroid and extrathyroid tissues, iodolipids are the mediators of iodine properties, through PPAR-gamma activation [11][12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Iodine Affects Differentiation and Migration Process in Trophoblastic Cells

Vidal

Rodríguez

Arroyo-Helguera

2015

Biol Trace Elem Res

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Iodine deficiency is associated with oxidative stress increase and preeclampsia during gestation, suggesting that iodine concentration plays an important role in the normal placenta physiology. The question raised is to analyze the effect of iodine deficiency on oxidative stress, viability, differentiation, and migration process and changes in the expression of differentiation and migration markers. Iodine deprivation was done using potassium perchlorate (KCLO4) to block sodium iodide symporter (NIS) transporter and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid DIDS to inhibit pendrine (PEN) transport for 3-48 h. Then trophoblast cells were treated with low iodine doses of 5-500 μM and high iodine doses of 100-5000 μM. Oxidative stress, viability, and human chorionic gonadotropin (hGC) were measured by colorimetric methods. Migration throphoblast cells were evaluated by both wound healing and Boyden chamber assays. Changes in mRNA expression were analyzed by real-time RT-PCR. Iodine deprivation induces a significant increase of reactive oxygen species (ROS), viability, and migration process vs control cells. We found a significant overregulation in the mRNA's peroxisome proliferator-activated receptor (PPAR-gamma), Snail, and matrix metalloproteinase-9 (MMP-9) mRNA's in cells deprived of iodine, as well as a down glial cell missing-1 (GCM-1) regulation, hGC, pregnancy-associated plasma protein-A (PAPP-A), and E-cadherin mRNA expression. The expression of hypoxic induction factor alpha (HIFα) mRNA does not change with iodine deprivation. In cells deprived of iodine, supplementing low iodine doses (5-500 μM) does not induce any significant changes in viability. However, ROS and migration process were decreased, although we found an increased human chorionic gonadotropin (hCG) secretion as a differentiation marker. In addition, we found that PPAR-gamma, Snail, and MPP-9 mRNAs expression are downregulated with low iodine doses, in contrast with GCM-1, PAPP-A, hGC, and E-cadherin that increase their expression vs cells deprived of iodine. High iodine doses (1000-5000 μM) have shown cytotoxic effects. Based on our results, iodine is important for keeping the proliferation/differentiation balance in the placenta.

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“…Thyroid VEGF is upregulated by estrogen, and thyroid weight, vascular area, and VEGF protein expression are lower in ovariectomized rats in comparison with sham-operated rats and ovariectomized rats treated with 17b-estradiol (de Araujo et al 2010). Interestingly, in PCCL3 cells, an increase in intracellular ROS, elicited by iodide deprivation, induces HIF-1a and VEGF protein expression, but concomitant treatment with the antioxidant N-acetyl-cysteine abolishes the effects of iodide deprivation (Gérard et al 2009). Thus, it is tempting to speculate that NOX4 could also be involved in the regulation of thyroid VEGF expression induced by estradiol and iodide deprivation.…”

Section: Estrogen Effects On Thyroid Redox Balancementioning

confidence: 99%

Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress?

Fortunato¹,

Ferreira²,

Hecht³

et al. 2014

Journal of Endocrinology

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Thyroid diseases, such as autoimmune disease and benign and malignant nodules, are more prevalent in women than in men, but the mechanisms involved in this sex difference is still poorly defined. H 2 O 2 is produced at high levels in the thyroid gland and regulates parameters such as cell proliferation, migration, survival, and death; an imbalance in the cellular oxidant-antioxidant system in the thyroid may contribute to the greater incidence of thyroid disease among women. Recently, we demonstrated the existence of a sexual dimorphism in the thyrocyte redox balance, characterized by higher H 2 O 2 production, due to higher NOX4 and Poldip2 expression, and weakened enzymatic antioxidant defense in the thyroid of adult female rats compared with male rats. In addition, 17b-estradiol administration increased NOX4 mRNA expression and H 2 O 2 production in thyroid PCCL3 cells. In this review, we discuss the possible involvement of oxidative stress in estrogenrelated thyroid pathophysiology. Our current hypothesis suggests that a redox imbalance elicited by estrogen could be involved in the sex differences found in the prevalence of thyroid dysfunctions.

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

Cited by 29 publications

References 44 publications

Investigation of iodine deficient state and iodine supplementation in patients with severe motor and intellectual disabilities on long-term total enteral nutrition

Investigation of iodine deficient state and iodine supplementation in patients with severe motor and intellectual disabilities on long-term total enteral nutrition

Iodine Affects Differentiation and Migration Process in Trophoblastic Cells

Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress?

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