55 research outputs found
Radiation and Thyroid Cancer
Radiation-induced damage is a complex network of interlinked signaling pathways, which may result in apoptosis, cell cycle arrest, DNA repair, and cancer. The development of thyroid cancer in response to radiation, from nuclear catastrophes to chemotherapy, has long been an object of study. A basic overview of the ionizing and non-ionizing radiation effects of the sensitivity of the thyroid gland on radiation and cancer development has been provided. In this review, we focus our attention on experiments in cell cultures exposed to ionizing radiation, ultraviolet light, and proton beams. Studies on the involvement of specific genes, proteins, and lipids are also reported. This review also describes how lipids are regulated in response to the radiation-induced damage and how they are involved in thyroid cancer etiology, invasion, and migration and how they can be used as both diagnostic markers and drug targets
Localization of nuclear actin in nuclear lipid microdomains of liver and hepatoma cells: Possible involvement of sphingomyelin metabolism
Nuclear actin has been implicated in different nuclear functions. In this work, its localization in nuclear membrane, chromatin
and nuclear lipid microdomains was investigated. The implication of sphingomyelin metabolism was studied.
Nuclear membrane, chromatin and nuclear lipid microdomains were purified from hepatocyte nuclei and H35 human hepatoma
cell nuclei. The presence of \u3b2-actin was analyzed with immunoblotting by using specific antibodies. Sphingomyelinase,
sphingomyelin-synthase, and phosphatidylcholine-specific phospholipase C activities were assayed by using radioactivity
sphingomyelin and phosphatidylcholine as substrate.
The results showed that \u3b2-actin is localized in nuclear lipid microdomains and it increases in cancer cells. Evidence is provided
to the difference of phosphatidylcholine and sphingomyelin metabolism in various subnuclear fractions of cancer cell
nuclei compared with normal cells. Our findings show increase of sphingomyelin-synthase and inhibition of sphingomyelinase
activity only in nuclear lipid microdomains.
Nuclear lipid microdomains, constituted by phosphatidylcholine, sphingomyelin and cholesterol, play a role as platform for
\u3b2-actin anchoring. Possible role of sphingomyelin metabolism in cancer cells is discussed
Hypovitaminosis D3, Leukopenia, and Human Serotonin Transporter Polymorphism in Anorexia Nervosa and Bulimia Nervosa
Mouse thyroid gland changes in aging: Implication of galectin-3 and sphingomyelinase
Prevalence of thyroid dysfunction and its impact on cognition in older people has been demonstrated, but many points remain unclarified. In order to study the effect of aging on the thyroid gland, we compared the thyroid gland of very old mice with that of younger ones. We have first investigated the changes of thyroid microstructure and the possibility that molecules involved in thyroid function might be associated with structural changes. Results from this study indicate changes in the height of the thyrocytes and in the amplitude of interfollicular spaces, anomalous expression/localization of thyrotropin, thyrotropin receptor, and thyroglobulin aging. Thyrotropin and thyrotropin receptor are upregulated and are distributed inside the colloid while thyroglobulin fills the interfollicular spaces. In an approach aimed at defining the behavior of molecules that change in different physiopathological conditions of thyroid, such as galectin-3 and sphingomyelinase, we then wondered what was their behavior in the thyroid gland in aging. Importantly, in comparison with the thyroid of young animals, we have found a higher expression of galectin-3 and a delocalization of neutral sphingomyelinase in the thyroid of old animals. A possible relationship between galectin-3, neutral sphingomyelinase, and aging has been discussed
Nuclear lipid microdomains regulate daunorubicin resistance in hepatoma cells
Daunorubicin is an anticancer drug, and cholesterol is involved in cancer progression, but
their relationship has not been defined. In this study, we developed a novel experimental model that
utilizes daunorubicin, cholesterol, and daunorubicin plus cholesterol in the same cells (H35) to search
for the role of nuclear lipid microdomains, rich in cholesterol and sphingomyelin, in drug resistance.
We find that the daunorubicin induces perturbation of nuclear lipid microdomains, localized in the
inner nuclear membrane, where active chromatin is anchored. As changes of sphingomyelin species in
nuclear lipid microdomains depend on neutral sphingomyelinase activity, we extended our studies
to investigate whether the enzyme is modulated by daunorubicin. Indeed the drug stimulated the
sphingomyelinase activity that induced reduction of saturated long chain fatty acid sphingomyelin
species in nuclear lipid microdomains. Incubation of untreated-drug cells with high levels of
cholesterol resulted in the inhibition of sphingomyelinase activity with increased saturated fatty acid
sphingomyelin species. In daunodubicin-treated cells, incubation with cholesterol reversed the action
of the drug by acting via neutral sphingomyelinase. In conclusion, we suggest that cholesterol and
sphingomyelin-forming nuclear lipid microdomains are involved in the drug resistance
The Impact of Long-Term Exposure to Space Environment on Adult Mammalian Organisms: A Study on Mouse Thyroid and Testis
Hormonal changes in humans during spaceflight have been demonstrated but the underlying mechanisms are still unknown. To clarify this point thyroid and testis/epididymis, both regulated by anterior pituitary gland, have been analyzed on long-term space-exposed male C57BL/10 mice, either wild type or pleiotrophin transgenic, overexpressing osteoblast stimulating factor-1. Glands were submitted to morphological and functional analysis
Why high cholesterol levels help hematological malignancies: role of nuclear lipid microdomains
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