The effect of low dose lipopolysaccharide on thyroid hormone-regulated actin cytoskeleton modulation and type 2 iodothyronine deiodinase activity in astrocytes

Xu, Ming; Iwasaki, Tadaaki; Shimokawa, Noriaki; Sajdel-Sulkowska, Elizabeth M.; Koibuchi, Noriyuki

doi:10.1507/endocrj.ej13-0294

Cited by 8 publications

(5 citation statements)

References 40 publications

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“…MI can decrease the level of TSH and FT4, which is poorly described in the context of glial development and physiology. However, thyroxin participates in the mediation of signals in astrocytes [130] and is essential for cells motility, especially glial cells and neurons [131]. MI reflects glial activation in patients with psychosis.…”

Section: Relationship Of Thyroid Hormones With the Results Of Neuroim...mentioning

confidence: 99%

Redefining the Cut-Off Ranges for TSH Based on the Clinical Picture, Results of Neuroimaging and Laboratory Tests in Unsupervised Cluster Analysis as Individualized Diagnosis of Early Schizophrenia

Śmierciak

Szwajca

Popiela

et al. 2022

JPM

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Thyroid abnormalities, including mild forms of hypothyroidism and hyperthyroidism, are reported as risk factors for the development of a number of neuropsychiatric disorders, including schizophrenia. The diagnostic process still takes into account the extreme ranges of the accepted reference values for serum TSH since the concentration of free thyroxine in the serum does not change by definition. TSH mU/L cut-off values in psychiatric patients are currently clinically considered in the case of extremely high serum TSH levels (>4.0 mU/L). The results obtained in this study suggest that the clinically significant value has a lower TSH cut-off point with an upper limit of 2–2.5 mU/L. The criteria for the differential diagnosis of patients with schizophrenia, however, mainly take into account statutory reference ranges without a background related to the history of thyroid diseases in the family. The results indicate the need to lower the upper cut-off values for TSH among patients with early psychosis, which is related to the potential clinical significance of the obtained values both in the field of clinical evaluation and neuroimaging and laboratory evaluation parameters. The cut-off points obtained with the prior available knowledge coincided with the values established in the unsupervised clustering method, which further confirms the legitimacy of their use in the individualized diagnosis strategy of schizophrenia.

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Section: Relationship Of Thyroid Hormones With the Results Of Neuroim...mentioning

confidence: 99%

Redefining the Cut-Off Ranges for TSH Based on the Clinical Picture, Results of Neuroimaging and Laboratory Tests in Unsupervised Cluster Analysis as Individualized Diagnosis of Early Schizophrenia

Śmierciak

Szwajca

Popiela

et al. 2022

JPM

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“…Hypothalamic control of appetite regulation and energy expenditure not only involves the hypothalamus but also the hypothalamic pituitary axis (HPT). Recent evidence indicates that the HPT axis can control food intake and effects on appetite and body weight is mediated by thyroid hormones and LPS has become important to appetite regulation [102] [103]. Interests in the neuroendocrine system, energy metabolism and peripheral cholesterol metabolism have increased with the strong genetic identification andinvolvement NPY in plasma cholesterol regulation.…”

Section: Dysregulation Of Neuropeptides and Endocrine Hormones By Lpsmentioning

confidence: 99%

Anti-Aging Genes Improve Appetite Regulation and Reverse Cell Senescence and Apoptosis in Global Populations

Martins¹

2016

AAR

125

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Appetite regulation by nutritional intervention is required early in life that involves the anti-aging gene Sirtuin 1 (Sirt 1) with Sirt 1 maintenance of other cellular anti-aging genes involved in cell circadian rhythm, senescence and apoptosis. Interests in anti-aging therapy with appetite regulation improve an individual's survival to metabolic disease induced by gene-environment interactions by maintenance of the anti-aging genes connected to the metabolism of bacterial lipopolysaccharides, drugs and xenobiotics. Interventions to the aging process involve early calorie restriction with appetite regulation connected to appropriate genetic mechanisms that involve mitochondrial biogenesis and DNA repair in neurons. In the aging process as the anti-aging genes are suppressed as a result of transcriptional dysregulation chronic disease accelerations and connected to insulin resistance, non-alcoholic fatty liver disease (NAFLD) and neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. Interests in the gene-environment interaction indicate that the anti-aging gene Sirt 1that regulates food intake has been repressed early in the aging process in various global populations. The connections between Sirt 1 and other anti-aging genes such as Klotho, p66Shc (longevity protein) and Forkhead box proteins (FOXO1/ FOXO3a) have been associated with programmed cell death and alterations in these anti-aging genesregulate glucose, lipid and amyloid beta metabolism that are important to various chronic diseases.

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“…For instance, apart from the canonic role of thyroid hormones mentioned above, novel THRs synthetic ligands might also modulate TRs action, and intra and extracellular signals can affect cell sensitivity to T3 influencing TRs gene expression, TRs translation and its transport into the nucleus, and the recruitment of co-activators/-inhibitors (21, 24, 47). Furthermore, thyroid hormones can show non-genomic actions by binding to cell surface or cytoplasmic receptors and by interacting with other signaling pathways (16, 21, 48). …”

Section: Thyroid Function During Brain Developmentmentioning

confidence: 99%

An Evo-Devo Approach to Thyroid Hormones in Cerebral and Cerebellar Cortical Development: Etiological Implications for Autism

2014

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The morphological alterations of cortical lamination observed in mouse models of developmental hypothyroidism prompted the recognition that these experimental changes resembled the brain lesions of children with autism; this led to recent studies showing that maternal thyroid hormone deficiency increases fourfold the risk of autism spectrum disorders (ASD), offering for the first time the possibility of prevention of some forms of ASD. For ethical reasons, the role of thyroid hormones on brain development is currently studied using animal models, usually mice and rats. Although mammals have in common many basic developmental principles regulating brain development, as well as fundamental basic mechanisms that are controlled by similar metabolic pathway activated genes, there are also important differences. For instance, the rodent cerebral cortex is basically a primary cortex, whereas the primary sensory areas in humans account for a very small surface in the cerebral cortex when compared to the associative and frontal areas that are more extensive. Associative and frontal areas in humans are involved in many neurological disorders, including ASD, attention deficit-hyperactive disorder, and dyslexia, among others. Therefore, an evo-devo approach to neocortical evolution among species is fundamental to understand not only the role of thyroid hormones and environmental thyroid disruptors on evolution, development, and organization of the cerebral cortex in mammals but also their role in neurological diseases associated to thyroid dysfunction.

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The effect of low dose lipopolysaccharide on thyroid hormone-regulated actin cytoskeleton modulation and type 2 iodothyronine deiodinase activity in astrocytes

Cited by 8 publications

References 40 publications

Redefining the Cut-Off Ranges for TSH Based on the Clinical Picture, Results of Neuroimaging and Laboratory Tests in Unsupervised Cluster Analysis as Individualized Diagnosis of Early Schizophrenia

Redefining the Cut-Off Ranges for TSH Based on the Clinical Picture, Results of Neuroimaging and Laboratory Tests in Unsupervised Cluster Analysis as Individualized Diagnosis of Early Schizophrenia

Anti-Aging Genes Improve Appetite Regulation and Reverse Cell Senescence and Apoptosis in Global Populations

An Evo-Devo Approach to Thyroid Hormones in Cerebral and Cerebellar Cortical Development: Etiological Implications for Autism

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