scholarly journals Effect of Preeclampsia on Ultrastructure of Thyroid Gland, Hepatic Type 1 Iodothyronine Deiodinase, and Thyroid Hormone Levels in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Yunlu Liu ◽  
Zhuping Xu ◽  
Yanqin Li ◽  
Wenyan Jiang ◽  
Ming Lan ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Close Correlation ◽  
Normal Pregnancy ◽  
Follicular Cells ◽  
Free Triiodothyronine ◽  
Pregnant Rats ◽  
Iodothyronine Deiodinase ◽  
Protein Levels ◽  
Thyroid Follicular Cells

Background. Although hypothyroidism during pregnancy may develop grave outcomes for both mothers and offspring, management of which is still a challenge due to the insufficient understanding of this disease. The close correlation between hypothyroidism and preeclampsia is well documented, suggesting that preeclampsia is a potential risk factor for the development of maternal hypothyroidism. However, the exact role of preeclampsia in gestational hypothyroidism is still obscure. Objective. In this study, we explored the possible mechanisms of the effect of preeclampsia on thyroid function of maternal rats. Methods. Thirty pregnant rats were randomly divided into normal pregnancy control (NOP), preeclampsia (PE), and preeclampsia supplemented with amlodipine besylate (PEAml). NG-Nitro-L-arginine-methyl ester was used to induce preeclamptic symptoms. On gestational day 21, rats were sacrificed, and then, the ultrastructure of the thyroid gland, type 1 iodothyronine deiodinase (Dio1) expression, and serum-free thyroxine (FT4), free triiodothyronine (FT3), and thyroid stimulation hormones (TSH) were assessed. Results. Compared to NOP rats, results of PE rats showed that thyroid follicular cells’ ultrastructure was damaged; both hepatic Dio1 mRNA and protein levels were decreased. Interestingly, these changes were ameliorated in PEAml rats. Additionally, FT4, FT3, and TSH levels have no significant differences among groups. Conclusion. These findings indicated that preeclampsia could disrupt synthesis, secretion, and metabolism function of thyroid hormones by damaging thyroid follicular cells and interfering Dio1 expression.

pax2.1is required for the development of thyroid follicles in zebrafish

Development ◽  
2002 ◽  
Vol 129 (15) ◽  
pp. 3751-3760 ◽  
Author(s):  
Thomas Wendl ◽  
Klaus Lun ◽  
Marina Mione ◽  
Jack Favor ◽  
Michael Brand ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Marker Gene ◽  
Follicular Cells ◽  
Hormone Production ◽  
Zebrafish Model ◽  
Hormone Synthesis ◽  
Larval Stages ◽  
Thyroid Follicular Cells ◽  
Thyroid Development

The thyroid gland is an organ primarily composed of endoderm-derived follicular cells. Although disturbed embryonic development of the thyroid gland leads to congenital hypothyroidism in humans and mammals, the underlying principles of thyroid organogenesis are largely unknown. In this study, we introduce zebrafish as a model to investigate the molecular and genetic mechanisms that control thyroid development. Marker gene expression suggests that the molecular pathways of early thyroid development are essentially conserved between fish and mammals. However during larval stages, we find both conserved and divergent features of development compared with mammals. A major difference is that in fish, we find evidence for hormone production not only in thyroid follicular cells, but also in an anterior non-follicular group of cells.We show that pax2.1 and pax8, members of the zebrafish pax2/5/8 paralogue group, are expressed in the thyroid primordium. Whereas in mice, only Pax8 has a function during thyroid development, analysis of the zebrafish pax2.1 mutant no isthmus (noi–/–) demonstrates that pax2.1 has a role comparable with mouse Pax8 in differentiation of the thyroid follicular cells. Early steps of thyroid development are normal in noi–/–, but later expression of molecular markers is lost and the formation of follicles fails. Interestingly, the anterior non-follicular site of thyroid hormone production is not affected in noi–/–. Thus, in zebrafish, some remaining thyroid hormone synthesis takes place independent of the pathway leading to thyroid follicle formation. We suggest that the noi–/– mutant serves as a new zebrafish model for hypothyroidism.

scholarly journals Type 1 and type 2 iodothyronine deiodinases in the thyroid gland of patients with 3,5,3′-triiodothyronine-predominant Graves' disease

2011 ◽  
Vol 164 (1) ◽  
pp. 95-100 ◽  
Author(s):  
Mitsuru Ito ◽  
Nagaoki Toyoda ◽  
Emiko Nomura ◽  
Yuuki Takamura ◽  
Nobuyuki Amino ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Mrna Level ◽  
Antithyroid Drug ◽  
High Serum ◽  
Graves Disease ◽  
Iodothyronine Deiodinase ◽  
Iodothyronine Deiodinases ◽  
Antithyroid Drug Therapy

Objective3,5,3′-triiodothyronine-predominant Graves' disease (T3-P-GD) is characterized by a persistently high serum T3 level and normal or even lower serum thyroxine (T4) level during antithyroid drug therapy. The source of this high serum T3 level has not been clarified. Our objective was to evaluate the contribution of type 1 and type 2 iodothyronine deiodinase (D1 (or DIO1) and D2 (or DIO2) respectively) in the thyroid gland to the high serum T3 level in T3-P-GD.MethodsWe measured the activity and mRNA level of both D1 and D2 in the thyroid tissues of patients with T3-P-GD (n=13) and common-type GD (CT-GD) (n=18) who had been treated with methimazole up until thyroidectomy.ResultsThyroidal D1 activity in patients with T3-P-GD (492.7±201.3 pmol/mg prot per h) was significantly higher (P<0.05) than that in patients with CT-GD (320.7±151.9 pmol/mg prot per h). On the other hand, thyroidal D2 activity in patients with T3-P-GD (823.9±596.4 fmol/mg prot per h) was markedly higher (P<0.005) than that in patients with CT-GD (194.8±131.6 fmol/mg prot per h). There was a significant correlation between the thyroidal D1 activity in patients with T3-P-GD and CT-GD and the serum FT3-to-FT4 ratio (r=0.370, P<0.05). Moreover, there was a strong correlation between the thyroidal D2 activity in those patients and the serum FT3-to-FT4 ratio (r=0.676, P<0.001).ConclusionsOur results suggest that the increment of thyroidal deiodinase activity, namely D1 and especially D2 activities, may be responsible for the higher serum FT3-to-FT4 ratio in T3-P-GD.

Expression of nitric oxide synthase III in human thyroid follicular cells: evidence for increased expression in hyperthyroidism

1997 ◽  
Vol 136 (6) ◽  
pp. 649-655 ◽  
Author(s):  
Ides M Colin ◽  
Peter Kopp ◽  
Jakob Zbären ◽  
André Häberli ◽  
William E Grizzle ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Thyroid Gland ◽  
Tsh Receptor ◽  
Human Thyroid ◽  
Graves Disease ◽  
Follicular Cells ◽  
Thyroid Follicular Cells ◽  
Hypothyroid Patients ◽  
Hyperthyroid Patients

Abstract Nitric oxide mediates a wide array of cellular functions in many tissues. It is generated by three known isoforms of nitric oxide synthases (NOS). Recently, the endothelial isoform, NOSIII, was shown to be abundantly expressed in the rat thyroid gland and its expression increased in goitrous glands. In this study, we analyzed whether NOSIII is expressed in human thyroid tissue and whether levels of expression vary in different states of thyroid gland function. Semiquantitative RT-PCR was used to assess variations in NOSIII gene expression in seven patients with Graves' disease, one with a TSH-receptor germline mutation and six hypothyroid patients (Hashimoto's thyroiditis). Protein expression and subcellular localization were determined by immunohistochemistry (two normal thyroids, five multinodular goiters, ten hyperthyroid patients and two hypothyroid patients). NOSIII mRNA was detected in all samples: the levels were significantly higher in tissues from hyperthyroid patients compared with euthyroid and hypothyroid patients. NOSIII immunoreactivity was detected in vascular endothelial cells, but was also found in thyroid follicular cells. In patients with Graves' disease, the immunostaining was diffusely enhanced in all follicular cells. A more intense signal was observed in toxic adenomas and in samples obtained from a patient with severe hyperthyroidism due to an activating mutation in the TSH receptor. In multinodular goiters, large follicles displayed a weak signal whereas small proliferative follicles showed intense immunoreactivity near the apical plasma membrane. In hypothyroid patients, NOSIII immunoreactivity was barely detectable. In summary, NOSIII is expressed both in endothelial cells and thyroid follicular cells. The endothelial localization of NOSIII is consistent with a role for nitric oxide in the vascular control of the thyroid. NOSIII expression in thyroid follicular cells and the variations in its immunoreactivity suggest a possible role for nitric oxide in thyrocyte function and/or growth. European Journal of Endocrinology 136 649–655

scholarly journals Mercury in the human thyroid gland: Potential implications for thyroid cancer, autoimmune thyroiditis, and hypothyroidism

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0246748
Author(s):  
Roger Pamphlett ◽  
Philip A. Doble ◽  
David P. Bishop
Keyword(s):  
Mass Spectrometry ◽  
Laser Ablation ◽  
Thyroid Gland ◽  
Toxic Metals ◽  
Inductively Coupled Plasma ◽  
Human Thyroid ◽  
Follicular Cells ◽  
Inductively Coupled ◽  
Thyroid Follicular Cells ◽  
Plasma Mass Spectrometry

Objective Mercury and other toxic metals have been suggested to be involved in thyroid disorders, but the distribution and prevalence of mercury in the human thyroid gland is not known. We therefore used two elemental bio-imaging techniques to look at the distribution of mercury and other toxic metals in the thyroid glands of people over a wide range of ages. Materials and methods Formalin-fixed paraffin-embedded thyroid tissue blocks were obtained from 115 people aged 1–104 years old, with varied clinicopathological conditions, who had thyroid samples removed during forensic/coronial autopsies. Seven-micron sections from these tissue blocks were used to detect intracellular inorganic mercury using autometallography. The presence of mercury was confirmed using laser ablation-inductively coupled plasma-mass spectrometry which can detect multiple elements. Results Mercury was found on autometallography in the thyroid follicular cells of 4% of people aged 1–29 years, 9% aged 30–59 years, and 38% aged 60–104 years. Laser ablation-inductively coupled plasma-mass spectrometry confirmed the presence of mercury in samples staining with autometallography, and detected cadmium, lead, iron, nickel and silver in selected samples. Conclusions The proportion of people with mercury in their thyroid follicular cells increases with age, until it is present in over one-third of people aged 60 years and over. Other toxic metals in thyroid cells could enhance mercury toxicity. Mercury can trigger genotoxicity, autoimmune reactions, and oxidative damage, which raises the possibility that mercury could play a role in the pathogenesis of thyroid cancers, autoimmune thyroiditis, and hypothyroidism.

scholarly journals Use of osmium-ferrocyanide treatment for improved lysosomal acid trimetaphosphatase reaction and subcellular detail in thyroid follicular cells.

1980 ◽  
Vol 28 (2) ◽  
pp. 183-186 ◽  
Author(s):  
A F Payer ◽  
C L Battle ◽  
R L Peake
Keyword(s):  
Heavy Metal ◽  
Thyroid Gland ◽  
Tissue Preservation ◽  
Follicular Cells ◽  
Enzyme Localization ◽  
Histochemical Reaction ◽  
Tissue Sections ◽  
Thyroid Follicular Cells ◽  
Secondary Tissue ◽  
Mouse Thyroid

The histochemical reaction for acid trimetaphosphatase in addition to secondary tissue treatment with an osmium-ferrocyanide mixture was used to study lysosomes and phagolysosomes in the mouse thyroid gland. The osmium-ferrocyanide postfixation enhanced reaction product localization, reduced diffuse reaction, and improved membrane contrast. In addition, the ultrathin tissue sections did not require heavy metal staining, thus eliminating potential stain artifacts due to precipitation. In view of the improved tissue preservation and enzyme localization, it is suggested that osmium-ferrocyanide postfixation be used after the acid trimetaphosphatase method.

scholarly journals SAT-LB78 TSH Is a Negative Modulator of Hippo Transcriptional Effectors

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Celia Fernández-Méndez ◽  
Pilar Santisteban
Keyword(s):  
Thyroid Gland ◽  
Hippo Pathway ◽  
Thyroid Tissue ◽  
Tissue Growth ◽  
Human Thyroid ◽  
In Vivo Model ◽  
Future Research ◽  
Follicular Cells ◽  
Thyroid Follicular Cells ◽  
The Hippo Pathway

Abstract Hippo signaling pathway regulation by hormonal signals acting through G-coupled receptors has been widely described. Modulation of processes such as tissue growth or differentiation by this pathway critically relies on the location and levels of its major effectors: the cofactors YAP/TAZ and the family TEAD of transcription factors. Despite this well-defined regulatory mechanism, little is known about the Hippo pathway in the thyroid gland. Thyrotropin (TSH), main factor for thyroid follicular cells differentiation, plays its role by interacting with its G-protein-coupled receptor (TSHR). High serum TSH levels are associated with hypothyroidism, characterized by a change in thyroid follicle morphology and inflammation of the thyroid gland. This led us to study if TSH could modulate the Hippo pathway.Rat thyroid follicular cells (PCCl3) were treated with TSH and forskolin, an adenylyl cyclase activator. By immunofluorescence and western blot, levels and subcellular location of the Hippo Pathway components were assessed in different conditions. An increase of the Hippo kinase MST1/2 and LATS1/2 was observed after TSH and forskolin treatments, corresponding to a downregulation of the transcriptional mediators of the pathway TAZ, YAP and Tead1. Especially remarkable is the translocation of YAP/TAZ from the nucleus, which involves a decrease in their activity.Next, we validated the results in an in vivo model generating hypothyroidism in 3-month-old male C57BL/6J by adding MMI (2-Mercapto-1-Methylimidazole) and perchlorate (KClO4) to their drinking water. After 2 weeks of treatment, we euthanized the animals, validated higher TSH serum levels and performed analysis of the Hippo components in the thyroid by immunohistochemistry. A reduction in the levels of the Hippo effectors TAZ, YAP and Tead1 was found in the thyroid slices from hypothyroid mice, confirming the in vitro results. In addition, evaluation of a human thyroid tissue microarray, including Hashimoto disease samples, led to a validation of the previously described TSH role.Hereby, we report a crosstalk by which TSH is increasing the kinase axis of the Hippo pathway thus decreasing the activity of its main transcriptional effectors in the nuclei. Future research of the role of these transcriptional effectors will be carry out to discern if their decrease could be associated with the morphology changes linked to hypothyroidism.

scholarly journals Bilateral thyroid follicular compact-cellular carcinoma in a llama

2019 ◽  
Vol 31 (6) ◽  
pp. 913-916
Author(s):  
Rodrigo A. Carrasco ◽  
Jolanda Verhoef ◽  
Carlos E. P. Leonardi ◽  
Emily E. Lanigan ◽  
Gregg P. Adams
Keyword(s):  
Thyroid Gland ◽  
Clinical Signs ◽  
Postmortem Examination ◽  
Follicular Cells ◽  
Regional Lymph Nodes ◽  
Thyroid Follicular Cells ◽  
Lama Glama ◽  
Cellular Carcinoma ◽  
Multiple Cysts ◽  
Cervical Area

An 18-y-old female llama ( Lama glama) in Saskatoon, Saskatchewan was examined during a routine herd check, and a mass was detected in the ventral cervical area just below the angle of the jaw. No clinical signs were evident except for the mass and chronic loss of body condition. Postmortem examination revealed bilateral enlargement of the thyroid gland with multiple cysts. Histopathology of the thyroid gland revealed follicular compact-cellular carcinoma lesions, with infiltration of neoplastic thyroid follicular cells in regional lymph nodes.

scholarly journals Primary Cilia Mediate TSH-Regulated Thyroglobulin Endocytic Pathways

2021 ◽  
Vol 12 ◽  
Author(s):  
Junguee Lee ◽  
Hae Joung Sul ◽  
Kun-Ho Kim ◽  
Joon Young Chang ◽  
Minho Shong
Keyword(s):  
Thyroid Gland ◽  
Primary Cilium ◽  
Untreated Control ◽  
Primary Cilia ◽  
Apical Surface ◽  
Follicular Cells ◽  
Thyroid Follicular Cells ◽  
Ciliary Signaling ◽  
Endocytic Pathways

Primary cilia are sensory organelles with a variety of receptors and channels on their membranes. Recently, primary cilia were proposed to be crucial sites for exocytosis and endocytosis of vesicles associated with endocytic control of various ciliary signaling pathways. Thyroglobulin (Tg) synthesis and Tg exocytosis/endocytosis are critical for the functions of thyroid follicular cells, where primary cilia are relatively well preserved. LRP2/megalin has been detected on the apical surface of absorptive epithelial cells, including thyrocytes. LRP2/megalin on thyrocytes serves as a Tg receptor and can mediate Tg endocytosis. In this study, we investigated the role of primary cilia in LRP2/megalin expression in thyroid gland stimulated with endogenous TSH using MMI-treated and Tg-Cre;Ift88flox/flox mice. LRP2/megalin expression in thyroid follicles was higher in MMI-treated mice than in untreated control mice. MMI-treated mice exhibited a significant increase in ciliogenesis in thyroid follicular cells relative to untreated controls. Furthermore, MMI-induced ciliogenesis accompanied increases in LRP2/megalin expression in thyroid follicular cells, in which LRP2/megalin was localized to the primary cilium. By contrast, in Tg-Cre;Ift88flox/flox mice, thyroid with defective primary cilia expressed markedly lower levels of LRP2/megalin. Serum Tg levels were elevated in MMI-treated mice and reduced in Tg-Cre;Ift88flox/flox mice. Taken together, these results indicate that defective ciliogenesis in murine thyroid follicular cells is associated with impaired LRP2/megalin expression and reduced serum Tg levels. Our results strongly suggest that primary cilia harbors LRP2/megalin, and are involved in TSH-mediated endocytosis of Tg in murine thyroid follicles.

Sign in / Sign up

Export Citation Format

Share Document