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Ahmed RG
Division
of Anatomy and Embryology, Zoology Department, Faculty of Science, Beni-Suef
University, Beni-Suef, Egypt
*Corresponding
author: Ahmed RG, Division of Anatomy and Embryology, Zoology Department, Faculty of
Science, Beni-Suef University, Beni-Suef, Egypt. Tel: +201091471828; Email: ahmedragab08@gmail.com
Received Date: 10 January, 2018; Accepted Date: 12, January, 2018; Published Date: 18 January, 2018
Editorial
Thyroid Hormones (THs) display key activities during
the ordinary development [1-53] through genomic and non-genomic actions [51]. Extra
nuclear or non-genomic actions of THs have been found in the cellular
organelles, cytoplasm and plasma membrane [51,54,55].
Also, these actions have comprised the activation of Mitogen Activated Protein
Kinase (ERK/MAPK) and Protein Kinases (PKA & PKC), modulation of glucose
transport and sodium, potassium and calcium ions, and regulation of Phospholipases
(PLC & PLD) [56,57]. Specifically, Thyroxine
(T4) can bind to a membrane integrin receptor (αVβ3)
inducing MAPK activity [58,59]. In addition, THs
regulate the behaviors of interferon-γ (IFN-γ) [60] and growth
factors, such as vascular growth factors [61, 62],
transforming growth factor-β (TGF-β) [63], and Epidermal
Growth Factor (EGF), by non-genomic mechanisms [49,64,65].
T4 can increase the levels of TGF-β and
EGF-induced the expression of c-fosand activation
of ERK1/2 in HeLa cells [63]. Thus, non-genomic
mechanisms of TH are not regularly stimulatory because of TH can inhibit the
actions of TGF-β and stimulate the
autocrine/paracrine effects of EGF [49].
On the other hand, THs can induce the action of
insulin growth factor I (IGF-I) on account of integrin αVβ3
has a cell surface receptor for THs and co receptor for IGF-I [49,66]. IGF-I supports the cellular growth, regulates
the glucose homeostasis, and stimulates the level of insulin sensitivity in the
biological tissues through paracrine, autocrine, and endocrine actions [40, 50]. More importantly, in the smooth muscle
cells, the action of IGF-I may be mediated by the receptors of integrinαVβ3 [67,68,49]. Thus, the nature of integrin as a
structural and functional may be very important to the actions of the muscles [69-72]. Recently, my group reported that T4
(subnanomolar free hormone concentration) prevents IGF-I stimulation of glucose
uptake and cellular proliferation[49]. This
action may be mediated by the crosstalk between the IGF-I receptor (IGF-IR) and
integrin αVβ3[68].
Thus, these data propose that the non-genomic actionof THscan show a significant role during the regular
development. Additional examinations are desired to distinguish the crosstalk
between THs and their non-genomic actions during the development. In addition,
several studies are needed to explore the interactions between the T4 and IGF-I
on the actions of phosphatidylinositol 3-kinase (PI3K) and ERK1/2 signal
transduction pathway in the glucose uptake and cell proliferation.
1. El-bakry AM, El-Ghareeb AW,Ahmed RG(2010) Comparative study of the effects of experimentally-induced
hypothyroidism and hyperthyroidism in some brain regions in albino rats.Int
JDevNeurosci 28: 371-389.
2. Ahmed RG(2011) Perinatal 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin exposure
alters developmental neuroendocrine system. Food Chem Toxicology 49: 1276-1284.
3. Ahmed RG (2012a)
Maternal-newborn thyroid dysfunction. In RG Ahmed(Ed)The Developmental
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5. Ahmed RG(2013) Early weaning PCB 95 exposure alters the neonatal
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Ahmed RG (2014)Editorial: Do PCBs modify the thyroid-adipokine axis during
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Ahmed RG (2015a) Hypothyroidism and brain development. In advances in hypothyroidism
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Ahmed RG (2015d) Developmental adipokines and
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11. Ahmed RG (2016a)Gestational dexamethasone alters fetal neuroendocrine
axis. Toxicology
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12. Ahmed RG (2016b) Neonatal polychlorinated
biphenyls-induced endocrine dysfunction. Ann. Thyroid Res 2: 34-35.
13. Ahmed RG (2016c) Maternal iodine deficiency and brain
disorders. Endocrinol MetabSyndr 5: 223.
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Thyroid adipokine dysfunction. Food Chem Toxicology 95: 168-174.
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thyroid diseases and GABAergic dysfunction. EC Neurology 8.1: 02-04.
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dysfunction. Arch Med 9: 4.
17. Ahmed RG (2017c) Anti-thyroid
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hypothyroidism and cytoskeleton dysfunction. Endocrinol MetabSyndr 6: 271.
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Arch Med 9: 2.
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prooxidant-antioxidant imbalance may be at higher risk for postpartum thyroid
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actions of thyroid-adipokines axis during development.Endocrinol MetabSyndr 6: 280.
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Journal of Research Studies in Zoology 3: 73-75.
25. Ahmed RG (2017k) Developmental
thyroid diseases and cholinergic imbalance.
International Journal of Research Studies in Zoology 3: 70-72.
26. Ahmed RG (2017l) Thyroid
diseases and developmental adenosinergic imbalance. Int J Clin Endocrinol 1: 053-055.
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risk for thyroid disease developing peripartum. Open Journal of Biomedical&
Life Sciences (Ojbili) 3: 01-06.
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Nutrition 11: 183-185.
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Int J of Res Studies in Medical and Health Sciences 2: 18-21.
31. Ahmed RG (2017r) Association between
hypothyroidism and renal dysfunctions.
International Journal of Research Studies in Medical and Health Sciences 2: 1-4.
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33.
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offspring: I- The development of the thyroid hormones-neurotransmitters and
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