Thyroid hormone synthesis requires adequate hydrogen peroxide (H2O2) production that is utilized as an oxidative agent during the synthesis of thyroxin (T4) and triiodothyronine (T3). Thyroid H2O2 is generated by a member of the family of NADPH oxidase enzymes (NOX-es), termed dual oxidase 2 (DUOX2). NOX/DUOX enzymes produce reactive oxygen species (ROS) as their unique enzymatic activity in a timely and spatially regulated manner and therefore, are important regulators of diverse physiological processes. By contrast, dysfunctional NOX/DUOX-derived ROS production is associated with pathological conditions. Inappropriate DUOX2-generated H2O2 production results in thyroid hypofunction in rodent models. Recent studies also indicate that ROS improperly released by NOX4, another member of the NOX family, are involved in thyroid carcinogenesis. This review focuses on the current knowledge concerning the redox regulation of thyroid hormonogenesis and cancer development with a specific emphasis on the NOX and DUOX enzymes in these processes.

H2O2 Metabolism in Normal Thyroid Cells and in Thyroid Tumorigenesis: Focus on NADPH Oxidases.

Targeting the pentose phosphate pathway increases reactive oxygen species and induces apoptosis in thyroid cancer cells.

Purpose: Our previous study demonstrated that SIRT6 is upregulated in papillary thyroid cancer (PTC) and enhances tumor aggressiveness. In this study, we further researched its influence in the Warburg effect. Methods: SIRT6-upregulated and downregulated BCPAP cells and negative control BCPAP-NC groups were generated with lentiviral vectors. In these two cell lines, reactive oxygen species (ROS) were detected by dichlorodihydrofluorescein diacetate. Expression of the key Warburg effect genes including GLUT1, HK2, GAPDH, PGK1, ENO1, PKM2 and LDHA was measured by quantitative real-time PCR and western blotting. Glucose uptake, lactate production and the ATP content of cells were detected with assay kits. The ROS scavenger N-acetylcysteine was used for treatment of BCPAP-SIRT6, and the same measurements as described above were detected again. Results: Compared with the BCPAP-NC group, expression of the key Warburg effect genes including Glut1, HK2 and GAPDH and their protein products was upregulated in the BCPAP-SIRT6 group, whereas BCPAP-shSIRT6 showed significant downregulation. Meanwhile, ROS, glucose uptake, lactate production and ATP content of the BCPAP-SIRT6 group were also significantly increased, and BCPAP-shSIRT6 showed significant downregulation. Furthermore, upregulation of key Warburg effect genes and glucose uptake, lactate production and ATP content were all rescued after treatment with ROS scavenger. Conclusion: SIRT6 promoted the Warburg effect of PTC cells via upregulation of ROS. Inhibition of ROS in SIRT6-upregulated cells could rescue activation of the Warburg effect.

/pdf/sirt6-promotes-the-warburg-effect-of-papillary-thyroid-41wtfmdmne.pdf

SIRT6 promotes the Warburg effect of papillary thyroid cancer cell BCPAP through reactive oxygen species.

Aging is associated with both muscle weakness and a loss of muscle mass, contributing towards overall frailty in the elderly. Aging skeletal muscle is also characterised by a decreasing efficiency in repair and regeneration, together with a decline in the number of adult stem cells. Commensurate with this are general changes in whole body endocrine signalling, in local muscle secretory environment, as well as in intrinsic properties of the stem cells themselves. The present review discusses the various mechanisms that may be implicated in these age-associated changes, focusing on aspects of cell-cell communication and long-distance signalling factors, such as levels of circulating growth hormone, IL-6, IGF1, sex hormones, and inflammatory cytokines. Changes in the local environment are also discussed, implicating IL-6, IL-4, FGF-2, as well as other myokines, and processes that lead to thickening of the extra-cellular matrix. These factors, involved primarily in communication, can also modulate the intrinsic properties of muscle stem cells, including reduced DNA accessibility and repression of specific genes by methylation. Finally we discuss the decrease in the stem cell pool, particularly the failure of elderly myoblasts to re-quiesce after activation, and the consequences of all these changes on general muscle homeostasis.

/pdf/changes-in-communication-between-muscle-stem-cells-and-their-16mfwz68n4.pdf

Changes in Communication between Muscle Stem Cells and their Environment with Aging.

Warburg found that tumor cells exhibit high-level glycolysis, even under aerobic condition, which is known as the 'Warburg effect'. As systemic changes in the entire metabolic network are gradually revealed, it is recognized that metabolic reprogramming has gone far beyond the imagination of Warburg. Metabolic reprogramming involves an active change in cancer cells to adapt to their biological characteristics. Thyroid cancer is a common endocrine malignant tumor whose metabolic characteristics have been studied in recent years. Some drugs targeting tumor metabolism are under clinical trial. This article reviews the metabolic changes and mechanisms in thyroid cancer, aiming to find metabolic-related molecules that could be potential markers to predict prognosis and metabolic pathways, or could serve as therapeutic targets. Our review indicates that knowledge in metabolic alteration has potential contributions in the diagnosis, treatment and prognostic evaluation of thyroid cancer, but further studies are needed for verification as well.

/pdf/metabolic-reprogramming-and-its-clinical-application-in-1dk7x4unor.pdf

Metabolic reprogramming and its clinical application in thyroid cancer (Review)

Acceleration of glycolysis is a characteristic of neoplasia. Previous studies have shown that a metabolic shift occurs in many tumors and correlates with a negative prognosis. The present study aimed to investigate the glycolytic profile of thyroid carcinoma cell lines. We investigated glycolytic and oxidative parameters of two thyroid carcinoma papillary cell lines (BCPAP and TPC1) and the non-tumor cell line NTHY-ori. All carcinoma cell lines showed higher rates of glycolysis efficiency, when compared to NTHY-ori, as assessed by a higher rate of glucose consumption and lactate production. The BCPAP cell line presented higher rates of growth, as well as elevated intracellular ATP levels, compared to the TPC1 and NTHY-ori cells. We found that glycolysis and activities of pentose phosphate pathway (PPP) regulatory enzymes were significantly different among the carcinoma cell lines, particularly in the mitochondrial hexokinase (HK) activity which was higher in the BCPAP cells than that in the TPC1 cell line which showed a balanced distribution of HK activity between cytoplasmic and mitochondrial subcellular localizations. However, TPC1 had higher levels of glucose‑6-phosphate dehydrogenase activity, suggesting that the PPP is elevated in this cell type. Using high resolution respirometry, we observed that the Warburg effect was present in the BCPAP and TPC1 cells, characterized by low oxygen consumption and high reactive oxygen species production. Overall, these results indicate that both thyroid papillary carcinoma cell lines showed a glycolytic profile. Of note, BCPAP cells presented some relevant differences in cell metabolism compared to TPC1 cells, mainly related to higher mitochondrial-associated HK activity.

/pdf/differential-glycolytic-profile-and-warburg-effect-in-2l9v4nlf6f.pdf

Differential glycolytic profile and Warburg effect in papillary thyroid carcinoma cell lines

We evaluated the effects of hypo- and hyperthyroid statuses during the initial phase of skeletal muscle regeneration in rats. To induce hypo- or hyperthyroidism, adult male Wistar rats were treated with methimazole (0.03%) or T4 (10 μg/100 g), respectively, for 10 days. Three days before sacrifice, a crush injury was produced in the solear muscles of one half of the animals, while the other half remained intact. T3, T4, TSH, and leptin serum levels were not affected by the injury. Serum T3 and T4 levels were significantly increased in hyperthyroid and hyper-injury animals. Hypothyroidism was confirmed by the significant increase in serum TSH levels in hypothyroid and hypo-injury animals. Injury increased cell infiltration and macrophage accumulation especially in hyperthyroid animals. Both type 2 and type 3 deiodinases were induced by lesion, and the opposite occurred with the type 1 isoform, at least in the control and hyperthyroid groups. Injury increased both MyoD and myogenin expression in all the studied groups, but only MyoD expression was increased by thyroidal status only at the protein level. We conclude that thyroid hormones modulate skeletal muscle regeneration possibly by regulating the inflammatory process, as well as MyoD and myogenin expression in the injured tissue.

Thyroid hormones regulate skeletal muscle regeneration after acute injury

O exercicio agudo e um desafio a homeostase e apos exercicio fisico intenso ocorre transiente linfopenia e imunossupressao. As moleculas de adesaao celular sao expressas na superficie dos leucocitos e das celulas endoteliais, tendo um papel fundamental nas interacoes entre linfocito e endotelio. O objetivo do presente estudo foi analisar a expressao de CD73, CD90 e CD105 em leucocitos apos corrida de alta intensidade. Dez homens jovens foram inscritos em uma corrida de 4 km e o sangue foi coletado 60 minutos antes, 5 minutos, 1, 3, 6 e 24 hs apos a o exercicio, para avaliacao hematologica e determinacao de marcadores de superficie celulares por citometria de fluxo. Foi utilizado o teste ANOVA de uma via com o teste de Dunnet's como post hoc para a analise estatistica. Os dados foram considerados diferentes estatisticamente quando p<0,05. Os leucocitos aumentaram 30% e os granulocitos 40 -- 70% apos 6h de exercicio fisico. Linfopenia foi observada 1 h apos o exercicio, como esperado. Monocitos, eosinofilos e basofilos, e outros parâmetros hematologicos nao se alteraram. Linfocitos T, linfocitos T helper e celulas citotoxicas aumentaram em resposta ao exercicio. Linfocitos B e as celulas exterminadoras naturais (natural killers) aumentaram imediatamente apos o exercicio. A celulas CD73 + aumentaram somente imediatamente apos o exercicio e as celulas CD90 + diminuiram 24h apos o exercicio. Podemos concluir que a corrida de alta intensidade induziu a resposta classica do sistema imuno-endocrino e e capaz de alterar o numero de celulas CD73 + e CD90 + .

/pdf/exercicio-de-corrida-de-alta-intensidade-altera-a-expressao-1uxxoyu108.pdf

Exercício de corrida de alta intensidade altera a expressão de thy-1 e ectonucleotidase na superfície de linfócitos

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Differential glycolytic profile and Warburg effect in papillary thyroid carcinoma cell lines

Thyroid hormones regulate skeletal muscle regeneration after acute injury

Exercício de corrida de alta intensidade altera a expressão de thy-1 e ectonucleotidase na superfície de linfócitos