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Thyroid Cell 2.0
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Thyroid Cell 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 14228

Special Issue Editor

Dr. Concetta Ambrosino

E-Mail Website
Guest Editor
Department of Science and Technology, University of Sannio, Via de Sanctis, 82100 Benevento, Italy
Interests: animal and cellular model of human disease; thyroid hormone signalling; infertility; EDC
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Thyroid hormones control the activity of several organs, and the functioning of the thyroid follicular cells is important for the health of the entire organism. Thyroid diseases and cancer are among the most frequent endocrine disorders and malignant diseases. Their incidence is continuously increasing worldwide, evidencing the necessity of continuous research in the field. The pathways injured in thyroid follicular cells and their disease specificity need further investigation. Genetic and environmental factors contribute to damaging thyroid follicular cells, and their interplay is still poorly characterized. The topic of this Special Issue is the characterization of thyroid disorders/cancers and of the promoting factors at follicular cell level in terms of morphological/functional and molecular changes. Studies using animal or cell culture models to investigate molecular mechanisms of thyroid diseases/cancers based on systems biology approaches will be published, which will lead to the characterization of molecular alterations representing novel diagnostic and prognostic molecular markers and therapeutic targets for thyroid disease/cancer. Researchers are encouraged to publish their work in this field, both with respect to endocrine thyroid diseases and thyroid carcinomas, including original articles or systematic reviews. 

Dr. Concetta Ambrosino
Guest Editor

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Keywords

  • thyroid cell
  • thyroid stem cell
  • thyroid diseases
  • thyroid cancer
  • cell biology
  • cell signaling
  • apoptosis
  • biomarker

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Published Papers (2 papers)

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Research

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17 pages, 1744 KiB  
Article
Genome-Wide Association Analysis and Genomic Prediction of Thyroglobulin Plasma Levels
by Nikolina Pleić, Mirjana Babić Leko, Ivana Gunjača, Thibaud Boutin, Vesela Torlak, Antonela Matana, Ante Punda, Ozren Polašek, Caroline Hayward and Tatijana Zemunik
Int. J. Mol. Sci. 2022, 23(4), 2173; https://doi.org/10.3390/ijms23042173 - 16 Feb 2022
Cited by 1 | Viewed by 2584
Abstract
Thyroglobulin (Tg) is an iodoglycoprotein produced by thyroid follicular cells which acts as an essential substrate for thyroid hormone synthesis. To date, only one genome-wide association study (GWAS) of plasma Tg levels has been performed by our research group. Utilizing recent advancements in [...] Read more.
Thyroglobulin (Tg) is an iodoglycoprotein produced by thyroid follicular cells which acts as an essential substrate for thyroid hormone synthesis. To date, only one genome-wide association study (GWAS) of plasma Tg levels has been performed by our research group. Utilizing recent advancements in computation and modeling, we apply a Bayesian approach to the probabilistic inference of the genetic architecture of Tg. We fitted a Bayesian sparse linear mixed model (BSLMM) and a frequentist linear mixed model (LMM) of 7,289,083 variants in 1096 healthy European-ancestry participants of the Croatian Biobank. Meta-analysis with two independent cohorts (total n = 2109) identified 83 genome-wide significant single nucleotide polymorphisms (SNPs) within the ST6GAL1 gene (p<5×10−8). BSLMM revealed additional association signals on chromosomes 1, 8, 10, and 14. For ST6GAL1 and the newly uncovered genes, we provide physiological and pathophysiological explanations of how their expression could be associated with variations in plasma Tg levels. We found that the SNP-heritability of Tg is 17% and that 52% of this variation is due to a small number of 16 variants that have a major effect on Tg levels. Our results suggest that the genetic architecture of plasma Tg is not polygenic, but influenced by a few genes with major effects. Full article
(This article belongs to the Special Issue Thyroid Cell 2.0)
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Review

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26 pages, 709 KiB  
Review
Environmental Factors That Affect Parathyroid Hormone and Calcitonin Levels
by Mirjana Babić Leko, Nikolina Pleić, Ivana Gunjača and Tatijana Zemunik
Int. J. Mol. Sci. 2022, 23(1), 44; https://doi.org/10.3390/ijms23010044 - 21 Dec 2021
Cited by 21 | Viewed by 11103
Abstract
Calciotropic hormones, parathyroid hormone (PTH) and calcitonin are involved in the regulation of bone mineral metabolism and maintenance of calcium and phosphate homeostasis in the body. Therefore, an understanding of environmental and genetic factors influencing PTH and calcitonin levels is crucial. Genetic factors [...] Read more.
Calciotropic hormones, parathyroid hormone (PTH) and calcitonin are involved in the regulation of bone mineral metabolism and maintenance of calcium and phosphate homeostasis in the body. Therefore, an understanding of environmental and genetic factors influencing PTH and calcitonin levels is crucial. Genetic factors are estimated to account for 60% of variations in PTH levels, while the genetic background of interindividual calcitonin variations has not yet been studied. In this review, we analyzed the literature discussing the influence of environmental factors (lifestyle factors and pollutants) on PTH and calcitonin levels. Among lifestyle factors, smoking, body mass index (BMI), diet, alcohol, and exercise were analyzed; among pollutants, heavy metals and chemicals were analyzed. Lifestyle factors that showed the clearest association with PTH levels were smoking, BMI, exercise, and micronutrients taken from the diet (vitamin D and calcium). Smoking, vitamin D, and calcium intake led to a decrease in PTH levels, while higher BMI and exercise led to an increase in PTH levels. In terms of pollutants, exposure to cadmium led to a decrease in PTH levels, while exposure to lead increased PTH levels. Several studies have investigated the effect of chemicals on PTH levels in humans. Compared to PTH studies, a smaller number of studies analyzed the influence of environmental factors on calcitonin levels, which gives great variability in results. Only a few studies have analyzed the influence of pollutants on calcitonin levels in humans. The lifestyle factor with the clearest relationship with calcitonin was smoking (smokers had increased calcitonin levels). Given the importance of PTH and calcitonin in maintaining calcium and phosphate homeostasis and bone mineral metabolism, additional studies on the influence of environmental factors that could affect PTH and calcitonin levels are crucial. Full article
(This article belongs to the Special Issue Thyroid Cell 2.0)
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