Thyroid Hormone Analogue Stimulates Keratinocyte Proliferation but Inhibits Cell Differentiation in Epidermis

Zhang, B.; Zhang, A.; Zhou, Xiaodong; Webb, Paul; Wang, He; Xia, Xuewei

doi:10.1177/039463201202500404

Cited by 15 publications

(11 citation statements)

References 28 publications

(47 reference statements)

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“…Topical application of TA 3 increases dermal thickness and prevents glucocorticoid-induced skin atrophy in mice and humans (Faergemann et al 2002, Yazdanparast et al 2006a, and stimulates procollagen synthesis and keratinocyte proliferation in human skin (Yazdanparast et al 2004, Zhang et al 2012, but has no beneficial effects on plaque psoriasis (Vahlquist et al 2004). …”

Section: Skinmentioning

confidence: 99%

Triiodothyroacetic acid in health and disease

Groeneweg

Peeters

Visser

et al. 2017

Journal of Endocrinology

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Thyroid hormone (TH) is crucial for development and metabolism of many tissues. The physiological relevance and therapeutic potential of TH analogs have gained attention in the field for many years. In particular, the relevance and use of 3,3′,5-triiodothyroacetic acid (Triac, TA 3 ) has been explored over the last decades. Although TA 3 closely resembles the bioactive hormone T 3 , differences in transmembrane transport and receptor isoformspecific transcriptional activation potency exist. For these reasons, the application of TA 3 as a treatment for resistance to TH (RTH) syndromes, especially MCT8 deficiency, is topic of ongoing research. This review is a summary of all currently available literature about the formation, metabolism, action and therapeutic applications of TA 3 .

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Section: Skinmentioning

confidence: 99%

Triiodothyroacetic acid in health and disease

Groeneweg

Peeters

Visser

et al. 2017

Journal of Endocrinology

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“…We observed that the levels of cyclins D1 and D3 were increased in the tumors grown in the hyperthyroid animals. Increased cyclin D1, which regulates the entry into the G1 phase of the cell cycle, has been widely linked to the regulation of the cell cycle by THs in various cell types (Ledda-Columbano et al 2006, Verga Falzacappa et al 2012, Zhang et al 2012. Many lines of evidence have indicated that cyclins D1 and D3 are involved in T-cell lymphomagenesis and are important molecular markers of oncogenic potential in T cell lymphomas (Teramoto et al 1999, Cheng et al 2008.…”

Section: Figurementioning

confidence: 99%

Thyroid status modulates T lymphoma growth via cell cycle regulatory proteins and angiogenesis

Sterle¹,

Valli²,

Cayrol³

et al. 2014

Journal of Endocrinology

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We have shown in vitro that thyroid hormones (THs) regulate the balance between proliferation and apoptosis of T lymphoma cells. The effects of THs on tumor development have been studied, but the results are still controversial. Herein, we show the modulatory action of thyroid status on the in vivo growth of T lymphoma cells. For this purpose, euthyroid, hypothyroid, and hyperthyroid mice received inoculations of EL4 cells to allow the development of solid tumors. Tumors in the hyperthyroid animals exhibited a higher growth rate, as evidenced by the early appearance of palpable solid tumors and the increased tumor volume. These results are consistent with the rate of cell division determined by staining tumor cells with carboxyfluorescein succinimidyl ester. Additionally, hyperthyroid mice exhibited reduced survival. Hypothyroid mice did not differ significantly from the euthyroid controls with respect to these parameters. Additionally, only tumors from hyperthyroid animals had increased expression levels of proliferating cell nuclear antigen and active caspase 3. Differential expression of cell cycle regulatory proteins was also observed. The levels of cyclins D1 and D3 were augmented in the tumors of the hyperthyroid animals, whereas the cell cycle inhibitors p16/INK4A (CDKN2A) and p27/Kip1 (CDKN1B) and the tumor suppressor p53 (TRP53) were increased in hypothyroid mice. Intratumoral and peritumoral vasculogenesis was increased only in hyperthyroid mice. Therefore, we propose that the thyroid status modulates the in vivo growth of EL4 T lymphoma through the regulation of cyclin, cyclin-dependent kinase inhibitor, and tumor suppressor gene expression, as well as the stimulation of angiogenesis.

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“…In addition, the treatment of rat cardiomyocytes with T3 increases the expression levels of cyclin D1 and thus induces the cell cycle progression [45]. In accordance with these results, the increment of Cyclin D1 has been widely linked to the TH-mediated regulation of the cell cycle in various cell types [46][47].…”

Section: Direct Action Of Ths On Tcl Cells Involves Both Genomic and mentioning

confidence: 53%

Classical and Non-Classical Thyroid Hormone Intracellular Pathways Involved in T Lymphoma Growth

Arcos¹,

Sterle²,

Cayrol³

et al. 2015

IEMAMC

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Thyroid hormones (THs) are important regulators of cell physiology. They are essential for the normal development and growth of mammals, especially for the neural differentiation and the regulation of the metabolism and the immune system. THs also induce the proliferation of several cell types. In human and murine T cell lymphomas (TCL) this effect involves the participation of genomic and nongenomic mechanisms as it was described by the use of free THs and non-cell permeable THs coupled to agarose (TH-ag). The classic actions of thyroid hormones involve the alteration of gene transcription via specific nuclear receptors. The discovery of other effects, independent of this classic mechanism, characterizes a new and non-classic mechanism that involves different signaling pathways. Both, free THs and TH-ag, activate protein kinase C, extracellular signal-regulated kinases and NF-kB and they increase the intracellular calcium levels. However, only the preincubation of T cells with free THs leads to an increased intracellular content of signaling enzymes. T lymphomas display high expression levels of both, the TH nuclear receptors (TRs) and the putative membrane receptor for THs, the integrin V 3, which has been demonstrated to be responsible for THs non-genomic actions. Here, we reviewed the mechanisms involved in THs modulation of the lymphocyte physiology, analyzing the interplay between genomic and nongenomic actions in T cells and its contribution in the development of lymphomas.

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Thyroid Hormone Analogue Stimulates Keratinocyte Proliferation but Inhibits Cell Differentiation in Epidermis

Cited by 15 publications

References 28 publications

Triiodothyroacetic acid in health and disease

Triiodothyroacetic acid in health and disease

Thyroid status modulates T lymphoma growth via cell cycle regulatory proteins and angiogenesis

Classical and Non-Classical Thyroid Hormone Intracellular Pathways Involved in T Lymphoma Growth

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