Thyroid hormone negatively regulates CDX2 and SOAT2 mRNA expression via induction of miRNA-181d in hepatic cells

Yap, Chun Wei; Sinha, Rohit Anthony; Ota, Sho; Katsuki, Masahito; Yen, Paul M.

doi:10.1016/j.bbrc.2013.09.116

Cited by 38 publications

(22 citation statements)

References 17 publications

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“…et al, 2012), increases mitochondrial membrane permeability (Maity et al, 2013), and activates transcription of several genes (Yap et al, 2013) and can regulate other cell functions.…”

Section: Enzymesmentioning

confidence: 99%

Thermogenesis and longevity in mammals. Thyroxin model of accelerated aging

Божков

Nikitchenko

2014

Experimental Gerontology

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“…et al, 2012), increases mitochondrial membrane permeability (Maity et al, 2013), and activates transcription of several genes (Yap et al, 2013) and can regulate other cell functions.…”

Section: Enzymesmentioning

confidence: 99%

Thermogenesis and longevity in mammals. Thyroxin model of accelerated aging

Божков

Nikitchenko

2014

Experimental Gerontology

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“…These mechanisms have also been shown to be mostly TH dependent negative regulation (11). The exact mechanisms involved in the negative regulation for the handful of genes during the feedback events have been studied for many years without much conclusion or consensus (12). For example, thyroid stimulating hormone gene α (TSHα) exhibits TH dependent transcription repression but the correlated negative TRE (nTRE) was poorly defined and showed different regulation pattern in different cellular environments (13-15).…”

Section: Introductionmentioning

confidence: 99%

Thyroid hormone-dependent epigenetic suppression of herpes simplex virus-1 gene expression and viral replication in differentiated neuroendocrine cells

Figliozzi

Chen

Balish

et al. 2014

Journal of the Neurological Sciences

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A global HSV-1 gene repression occurs during latency in sensory neurons where most viral gene transcriptions are suppressed. The molecular mechanisms of gene silencing and how stress factors trigger the reactivation are not well understood. Thyroid hormones are known to be altered due to stress, and with its nuclear receptor impart transcriptional repression or activation depending upon the hormone level. Therefore we hypothesized that triiodothyronine (T3) treatment of infected differentiated neuron like cells would reduce the ability of HSV-1 to produce viral progeny compared to untreated infected cells. Previously we identified putative thyroid hormone receptor elements (TREs) within the promoter regions of HSV-1 thymidine kinase (TK) and other key genes. Searching for a human cell line that can model neuronal HSV-1 infection, we performed HSV-1 infection experiments on differentiated human neuroendocrine cells, LNCaP. Upon androgen deprivation these cells undergo complete differentiation and exhibit neuronal-like morphology and physiology. These cells were readily infected by our HSV-1 recombinant virus, expressing GFP and maintaining many processes iconic of dendritic morphology. Our results demonstrated that differentiated LNCaP cells produced suppressive effects on HSV-1 gene expression and replication compared to its undifferentiated counterpart and T3 treatment have further decreased the viral plaque counts compared to untreated cells. Upon washout of the T3 viral plaque counts were restored, indicating an increase of viral replication. The qRT-PCR experiments using primers for TK showed reduced expression under T3 treatment. ChIP assays using a panel of antibodies for H3 lysine 9 epigenetic marks showed increased repressive marks on the promoter regions of TK. In conclusion we have demonstrated a T3 mediated quiescent infection in differentiated LNCaP cells that has potential to mimic latent infection. In this HSV-1 infection model thyroid hormone treatment caused decreased viral replication, repressed TK expression and increased repressive histone tail marks on the TK promoter.

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“…Thus, when MYH6 is induced by T 3 the production of the miRNA leads to the coincidental down-regulation of MYH7. Similarly in the liver, T 3 has the ability to induce the miRNA - 181d which in turn down regulates the expression of two targets SOAT and CDX2 [91]. Based on the ability of T 3 to regulate miRNAs in a variety of tissues this mechanism is likely to be highly conserved.…”

Section: Negative Regulation By Thyroid Hormonementioning

confidence: 99%

The actions of thyroid hormone signaling in the nucleus

Vella

Hollenberg

2017

Molecular and Cellular Endocrinology

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Thyroid hormones are a critical regulator of mammalian physiology. Much of their action is due to effects in the nucleus where T3 engages thyroid hormone receptor isoforms to mediate its effects. In order to function properly the TR isoforms must be recruited to regulatory sequences within genes that they up-regulate. On these positive regulated target genes the TR can activate or repress depending upon whether the receptor is bound to T3 or not and the type of co-regulatory proteins present in that cell type. In contrast to T3 mediated activation, the mechanism by which the TR represses transcription in the presence of T3 remains unclear. Herein we will review the components of the transcriptional response to T3 within the nucleus and attempt to highlight the outstanding questions in the field.

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Thyroid hormone negatively regulates CDX2 and SOAT2 mRNA expression via induction of miRNA-181d in hepatic cells

Cited by 38 publications

References 17 publications

Thermogenesis and longevity in mammals. Thyroxin model of accelerated aging

Thermogenesis and longevity in mammals. Thyroxin model of accelerated aging

Thyroid hormone-dependent epigenetic suppression of herpes simplex virus-1 gene expression and viral replication in differentiated neuroendocrine cells

The actions of thyroid hormone signaling in the nucleus

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