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ARC Journal of Diabetes and Endocrinology
Volume-4 Issue-1, 2018, Page No: 5-8
DOI: http://dx.doi.org/10.20431/2455-5983.0401002

Genomic Actions of Thyroid Hormones during Development

Ahmed R.G

Division of Anatomy and Embryology, Zoology Department, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt.

Citation : Ahmed R.G, "Genomic Actions of Thyroid Hormones during Development" ARC Journal of Diabetes and Endocrinology 2018; 4(1) : 5-8.

Copyright : © 2018 Authors. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Keywords: Genomic Actions,Thyroid Hormones,Development,Diabetes and Endocrinology


Rapid Communications

Thyroid hormones (THs) exhibit crucial activities during the development (El-bakry et al., 2010; Ahmed, 2011, 2012a,b, 2013, 2014, 2015a-c, 2016a-d, 2017a-u & 2018a-c; Ahmed et al., 2008, 2010, 2012, 2013a,b, 2014; 2015a,b& 2018a,b; Ahmed and Ahmed, 2012; Ahmed and Incerpi, 2013;Van Hercket al., 2013; Ahmed and El-Gareib, 2014,Incerpi et al., 2014; Can delotti et al., 2015; De Vito et al., 2015; El-Ghareeb et al., 2016; Ahmed and El-Gareib, 2017) via the nuclear and extra nuclear actions (De Vito et al., 2015).THs are released by the thyroid gland to the circulation where they are carried bound to proteins such as thyroxin binding globulin (TBG), transthyretin (TTR) or serum albumin (Shi et al., 2002). The level of albumin, which has the lowest thyroxine (T4) affinity and enables a fast release of T4 (Schussler, 2002), gradually decreases during pregnancy (Larsson et al., 2008). TBG is an active carrier and has a possibility to switch between the high-affinity and the low-affinity form (Zhou et al., 2006). TBG levels are the highest in the second and third trimester of pregnancy (Glinoer et al., 1990; Glinoer, 1997; Ahmed, 2012a) and the same holds true for TH-binding ratio (Lee et al., 2009) and thyroid-binding capacity (Kurioka et al., 2005), which decreases as soon as 3-4 days after delivery.

On the other hand, genomic actions of THs have been found inside the nucleus (Ahmed, 2012b). THs (3,5,3'-triiodothyronine (T3) and T4) arrive to the cell via transporter such as the organic anion transporter family (OATPs) and monocarboxylate transporter 8 (MCT8). Then, deiodinases (DI, and II) convert T4 (inactive form) to T3 (active form) (Ahmed et al., 2008; De Vito et al., 2011). At that point, T3 binds to thyroid receptors (TRs; TRα and TRβ), that stimulate transcription by binding, generally as heterodimers with the retinoid X receptor (RXR) (Bassett et al., 2003), to TH response elements (TREs) situated in regulatory regions of target genes (Chen et al., 2011). Its activity is controlled by an exchange of corepressor (CoR) and co activator (CoA) complexes. Negative TREs (nTRE) can facilitate ligand-dependent transcriptional repression (Contreras-Jurado et al., 2011). TRs can also adjust the actions of genes that do not comprise a TRE via cross-talk with other transcription factors (TF) that modulate target gene expression (Blair et al., 1999; Sirakov et al., 2011). Both co-regulators and receptors are goals for phosphorylation by signal transduction pathways motivated by hormones and growth factors (Chen et al., 2011; Contreras-Jurado et al., 2011).The nuclear actions of T3 are sensitive to inhibitors of transcription and translation and have a latency of hours to days (Yen, 2001; Ahmed, 2012a).Thus, the genomic action of THs can show significant roles during the cellular proliferations and differentiations. A better understanding of these mechanisms would also permit us to refine the timing and dosage of the increase in levothyroxine (L-T4) therapy in hypothyroid pregnant women and to establish whether T4 on its own is indeed the best form of TH replacement in pregnancy. Further studies are required to recognize the crosstalk between THs, their genomic actions and growth factors during the development.


References

  1. Ahmed R.G., 2017c.Maternal dioxin and fetal neuroendocrine dysfunction. Merit Research Journal of Medicine and Medical Sciences, Vol. 5(10) pp. xxx-xxx.
  2. Ahmed, O.M., Abd El-Tawab, S.M., Ahmed, R.G., 2010. Effects of experimentally induced maternal hypothyroidism and hyperthyroidism on the development of rat offspring: I- The development of the thyroid hormones- neurotransmitters and adenosinergic system interactions. Int. J. Dev. Neurosci. 28, 437-454.
  3. Ahmed, O.M., Ahmed, R.G., 2012. Hypothyroidism. In A New Look At Hypothyroidism. Dr. D. Springer (Ed.), ISBN: 978-953-51-0020-1), In Tech Open Access Publisher, Chapter 1, pp. 1-20.
  4. Ahmed, O.M., Ahmed, R.G., El-Gareib, A.W., El-Bakry, A.M., Abd El-Tawaba, S.M., 2012. Effects of experimentally induced maternal hypothyroidism and hyperthyroidism on the development of rat offspring: II-The developmental pattern of neurons in relation to oxidative stress and antioxidant defense system. Int. J. Dev. Neurosci. 30, 517–537.
  5. Ahmed, O.M., El-Gareib, A.W., El-bakry, A.M., Abd El-Tawab, S.M., Ahmed, R.G., 2008. Thyroid hormones states and brain development interactions. Int. J. Dev. Neurosci. 26(2), 147-209. Review.
  6. Ahmed, R.G., 2011. Perinatal 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin exposure alters developmental neuroendocrine system. Food Chem. Toxicology, 49, 1276–1284.
  7. Ahmed, R.G., 2012a. Maternal-newborn thyroid dysfunction. In the Developmental Neuro endocrinology, pp. 1-369. Ed R.G. Ahmed. Germany: LAP LAMBERT Academic Publishing GmbH & Co KG.
  8. Ahmed, R.G., 2012b. Maternal-fetal thyroid interactions, Thyroid Hormone, Dr. N.K. Agrawal (Ed.), ISBN: 978-953-51-0678-4, In Tech Open Access Publisher, Chapter 5, pp. 125-156.
  9. Ahmed, R.G., 2013. Early weaning PCB 95 exposure alters the neonatal endocrine system: thyroid adipokine dysfunction. J. Endocrinol. 219 (3), 205-215.
  10. Ahmed, R.G., 2014. Editorial: Do PCBs modify the thyroid-adipokine axis during development? Annals Thyroid Res. 1(1), 11-12.
  11. Ahmed, R.G., 2015a. Chapter 1: Hypothyroidism and brain development. In advances in hypothyroidism treatment. Avid Science Borsigstr.9, 10115 Berlin, Berlin, Germany. Avid Science Publications level 6, Melange Towers, Wing a, Hitec City, Hyderabad, Telangana, India. pp. 1-40.
  12. Ahmed, R.G., 2015b. Hypothyroidism and brain developmental players. Thyroid Research J. 8(2), 1-12.
  13. Ahmed, R.G., 2015c. Editorials and Commentary: Maternofetal thyroid action and brain development. J. of Advances in Biology; 7(1), 1207-1213.
  14. Ahmed, R.G., 2015d. Developmental adipokines and maternal obesity interactions. J. of Advances in Biology; 7(1), 1189-1206.
  15. Ahmed, R.G., 2016a. Gestational dexamethasone alters fetal neuro endocrine axis. Toxicology Letters, 258, 46–54.
  16. Ahmed, R.G., 2016b. Neonatal polychlorinated biphenyls-induced endocrine dysfunction. Ann. Thyroid. Res. 2 (1), 34-35.
  17. Ahmed, R.G., 2016c. Maternal iodine deficiency and brain disorders. Endocrinol. Metab.Syndr.5, 223. http://dx.doi.org/ 10.4172/ 2161-1017.1000223.
  18. Ahmed, R.G., 2016d. Maternal bisphenol A alters fetal endocrine system: Thyroid adipokine dysfunction. Food Chem. Toxicology, 95, 168-174.
  19. Ahmed, R.G., 2017a. Developmental thyroid diseases and GABAergic dysfunction. EC Neurology 8.1, 02-04.
  20. Ahmed, R.G., 2017b. Hyperthyroidism and developmental dysfunction. Arch Med. 9, 4.
  21. Ahmed, R.G.,2017c. Anti-thyroid drugs may be at higher risk for perinatal thyroid disease. EC Pharmacology and Toxicology 4.4, 140-142.
  22. Ahmed, R.G., 2017d. Perinatal hypothyroidism and cytoskeleton dysfunction. Endocrinol Metab Syndr 6, 271.doi:10.4172/2161-1017.1000271
  23. Ahmed, R.G., 2017e. Developmental thyroid diseases and monoaminergic dysfunction. Advances in Applied Science Research 8(3), 01-10.
  24. Ahmed, R.G.,2017f.Hypothyroidism and brain development .J. Anim Res Nutr.2(2), 13.
  25. Ahmed, R.G.,2017g. Antiepileptic drugs and developmental neuro endocrine dysfunction: Every why has A Wherefore. Arch Med 9(6), 2.
  26. Ahmed, R.G.,2017h. Gestational prooxidant-antioxidant imbalance may be at higher risk for postpartum thyroid disease. Endocrinol Metab Syndr 6, 279. doi:10.4172/2161-1017.1000279.
  27. Ahmed, R.G.,2017i. Synergistic actions of thyroid- adipokines axis during development. Endocrinol Metab Syndr 6, 280.doi: 10.4172/ 2161-1017.1000280.
  28. Ahmed, R.G.,2017j. Thyroid-insulin dysfunction during development. International Journal of Research Studies in Zoology 3(4), 73-75. DOI: http://dx.doi.org/10.20431/2454-941X.0304010.
  29. Ahmed, R.G.,2017k. Developmental thyroid diseases and cholinergic imbalance. International Journal of Research Studies in Zoology 3(4), 70-72. DOI: http://dx.doi.org/ 10.20431/2454-941X. 03040 09.
  30. Ahmed, R.G.,2017l. Thyroid diseases and developmental adenosinergic imbalance.Int J ClinEndocrinol 1(2), 053-055.
  31. Ahmed, R.G.,2017m.Maternal anticancer drugs and fetal neuroendocrine dysfunction in experimental animals.EndocrinolMetabSyndr 6, 281.doi:10.4172/2161-1017.1000281.
  32. Ahmed, R.G.,2017n. Letter: Gestational dexamethasone may be at higher risk for thyroid disease developing peripartum. Open Journal Of Biomedical & Life Sciences (Ojbili) 3(2), 01-06.
  33. Ahmed, R.G., 2017o.Deiodinases and developmental hypothyroidism. EC Nutrition 11.5, 183-185.
  34. Ahmed, R.G., 2017p.Maternofetal thyroid hormones and risk of diabetes. Int. J. of Res. Studies in Medical and Health Sciences 2(10), 18-21.
  35. Ahmed, R.G., 2017r.Association between hypothyroidism and renal dysfunctions. International Journal of Research Studies in Medical and Health Sciences 2(11), 1-4.
  36. Ahmed, R.G., 2017s.Maternal hypothyroidism and lung dysfunction. International Journal of Research Studies in Medical and Health Sciences 2(11), 8-11.
  37. Ahmed, R.G., 2017t.Endocrine disruptors; possible mechanisms for inducing developmental disorders. International journal of basic science in medicine (IJBSM) 2(4), xx-xx. (in press)
  38. Ahmed, R.G., 2017u.Maternal thyroid hormones trajectories and neonatal behavioral disorders. ARC Journal of Diabetes and Endocrinology 3(2), 18-21.
  39. Ahmed, R.G.,2018a. Maternal hypothyroidism and neonatal testicular dysfunction. International Journal of Research Studies in Medical and Health Sciences 3(1), 8-12.
  40. Ahmed, R.G., 2018b. Maternal thyroid disorders and bone maldevelopment: Are you ready to take risks for your off¬spring? J Pharma PharmaSci (JPPS) in press. DOI: 10.29011/2574-7711. 100058.
  41. Ahmed, R.G.,2018c. Non-genomic actions of thyroid hormones during development. App ClinPharmacolToxicol: ACPT-108. DOI: 10.29011/ACPT-109. 100008.
  42. Ahmed, R.G., Abdel-Latif, M., Ahmed F., 2015b.Protective effects of GM-CSF in experimental neonatal hypothyroidism. International Immunopharmacology 29, 538–543.
  43. Ahmed, R.G., Abdel-Latif, M., Mahdi, E., El-Nesr, K., 2015a. Immune stimulation improves endocrine and neural fetal outcomes in a model of maternofetal thyrotoxicosis. Int. Immunopharmacol. 29, 714-721.
  44. Ahmed, R.G., Davis, P.J., Davis, F.B., De Vito, P., Farias, R.N., Luly, P., Pedersen, J.Z., Incerpi, S., 2013b. Nongenomic actions of thyroid hormones: from basic research to clinical applications. An update. Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry, 13(1), 46-59.
  45. Ahmed, R.G., El-Gareib, A.W. 2014.Lactating PTU exposure: I- Alters thyroid-neural axis in neonatal cerebellum. Eur. J. of Biol. and Medical Sci. Res. 2(1), 1-16.
  46. Ahmed, R.G., El-Gareib, A.W., 2017.Maternal carbamazepine alters fetal neuroendocrine-cytokines axis. Toxicology 382, 59–66.
  47. Ahmed, R.G., El-Gareib, A.W., Incerpi, S., 2014. Lactating PTU exposure: II- Alters thyroid-axis and prooxidant-antioxidant balance in neonatal cerebellum. Int. Res. J. of Natural Sciences 2(1), 1-20.
  48. Ahmed, R.G.,El-Gareib, A.W., Shaker, H.M., 2018a.Gestational 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126) exposure disrupts fetoplacental unit: Fetal thyroid-cytokines dysfunction. Life Sciences 192, 213– 220.
  49. Ahmed, R.G., Incerpi, S., 2013. Gestational doxorubicin alters fetal thyroid–brain axis. Int. J. Devl. Neuroscience 31, 96–104.
  50. Ahmed, R.G., Incerpi, S., Ahmed, F., Gaber, A., 2013a. The developmental and physiological interactions between free radicals and antioxidant: Effect of environmental pollutants. J. of Natural Sci. Res. 3(13), 74-110.
  51. Ahmed, R.G.,Walaa G.H., Asmaa F.S., 2018b.Suppressive effects of neonatal bisphenol A on the neuroendocrine system.Toxicology and Industrial Health Journal (in press).
  52. Bassett, J.H.D., Harvey, C.B., Williams, G.R., 2003. Mechanisms of thyroid hormone receptorspecific nuclear and extra nuclear actions.Mol. and Cell.Endocrinol. 213, 1–11.
  53. Blair, A.S., Hajduch, E., Litherland, G.J., Hundal, H.S., 1999. Regulation of glucose transport and glycogen synthesis in L6 muscle cells during oxidative stress. Evidence for cross-talk between the insulin and SAPK2/p38 mitogen-activated protein kinase signaling pathways. J. Biol. Chem. 274, 36293–36299.
  54. Candelotti, E., De Vito, P., Ahmed, R.G., Luly, P., Davis, P.J., Pedersen, J.Z., Lin, H-Y., Incerpi, I., 2015. Thyroid hormones crosstalk with growth factors: Old facts and new hypotheses. Immun., Endoc.&Metab. Agents in Med. Chem., 15, 71-85.
  55. Chen, C., Zhou, Z., Zhong, M., Li, M., Yang, X., Zhang, Y., Wang, Y., Wei, A., Qu, M., Zhang, L., Xu, S., Chen, S., Yu, Z., 2011. Excess thyroid hormone inhibits embryonic neural stem/progenitor cells proliferation and maintenance through STAT3 signaling pathway. Neurotox. Res. 20, 15-25.
  56. Contreras-Jurado, C., Garcia-Serrano, L., Gomez-Ferreria, M., Costa, C., Paramio, J.M., Aranda, A., 2011.The thyroid hormone receptors as modulators of skin proliferation and inflammation. J. Biol. Chem. 286, 24079– 24088.
  57. De Vito, P., Candelotti, E., Ahmed, R.G., Luly, P., Davis, P.J., Incerpi, S., Pedersen, J.Z., 2015.Role of thyroid hormones in insulin resistance and diabetes. Immun., Endoc.&Metab. Agents in Med. Chem., 15, 86-93.
  58. De Vito, P., Incerpi, S., Pedersen, J.Z., Luly, P., Davis, F.B., Davis, P.J., 2011.Thyroid hormones as modulators of immune activities at the cellular level. Thyroid 21, 879-890.
  59. El-bakry, A.M., El-Ghareeb, A.W.,Ahmed, R.G., 2010.Comparative study of the effects of experimentally-induced hypothyroidism and hyperthyroidism in some brain regions in albino rats.Int. J. Dev. Neurosci. 28, 371-389.
  60. El-Ghareeb, A.A., El-Bakry, A.M., Ahmed, R.G., Gaber, A., 2016.Effects of zinc supplementation in neonatal hypothyroidism and cerebellar distortion induced by maternal carbimazole. Asian Journal of Applied Sciences 4(04), 1030-1040.
  61. Glinoer, D., 1997. The regulation of thyroid function in pregnancy: pathways of endocrine adaptation from physiology to pathology. Endocr. Rev. 18(3), 404–433.
  62. Glinoer, D., De Nayer, P., Bourdoux, P., 1990.Regulation of maternal thyroid during pregnancy. J. Clin. Endocrinol.Metab. 71(2), 276–287.
  63. Incerpi, S., Hsieh, M-T., Lin, H-Y., Cheng, G-Y., De Vito, P., Fiore, A.M., Ahmed, R.G., Salvia, R., Candelotti, E., Leone, S., Luly, P., Pedersen, J.Z., Davis, F.B., Davis, P.J., 2014. Thyroid hormone inhibition in L6 myoblasts of IGF-I-mediated glucose uptake and proliferation: new roles for integrin αvβ3. Am. J. Physiol. Cell Physiol. 307, C150–C161.
  64. Kurioka, H., Takahashi, K., Miyazaki, K., 2005. Maternal thyroid function during pregnancy and puerperal period.Endocr. J. 52(5), 587–591.
  65. Larsson, A., Palm, M., Hansson, L.O., Axelsson, O., 2008. Reference values for clinical chemistry tests during normal pregnancy. BJOG 115(7), 874– 881.
  66. Lee, R.H., Spencer, C.A., Mestman, J.H., 2009. Free T4 immunoassays are flawed during pregnancy. Am. J. Obstet. Gynecol. 200(3), e1–e6.
  67. Schussler, G.C., 2000. The thyroxine-binding proteins. Thyroid 10(2),141-149.
  68. Shi, Y-B., Ritchieb, J.W.A., Taylor, P.M., 2002. Complex regulation of thyroid hormone action: multiple opportunities for pharmacological intervention. Pharmacol.& Therapeutics 94, 235-251.
  69. Sirakov, M., Plateroti, M., 2011. The thyroid hormones and their nuclear receptors in the gut: From developmental biology to cancer. BiochimicaetBiophysicaActa 1812, 938-946.
  70. Van Herck, S.L.J., Geysens, S., Bald, E., Chwatko, G., Delezie, E., Dianati, E., Ahmed, R.G., Darras, V.M., 2013.Maternal transfer of methimazole and effects on thyroid hormone availability in embryonic tissues.Endocrinol. 218, 105-115.
  71. Yen, P.M.,2001. Physiological and molecular basis of thyroid hormone action. Physiol. Rev. 81(3), 1097-1126.
  72. Zhou, A., Wei, Z., Read, R.J., Carrell, R.W., 2006. Structural mechanism for the carriage and release of thyroxine in the blood. Proc. Natl Acad. Sci. USA 103(36), 13321-13326.

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