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3. Long-Term Exposure to Cadmium Causes Hepatic Iron Deficiency through the Suppression of Iron-Transport-Related Gene Expression in the Proximal Duodenum.

Author

Tokumoto, Maki, Lee, Jin-Yong, Fujiwara, Yasuyuki, and Satoh, Masahiko

Subjects
IRON deficiency, GENE silencing, GENE expression, CADMIUM, POLLUTANTS
Abstract

Cadmium (Cd) is an environmental pollutant that damages various tissues. Cd may cause a depletion of iron stores and subsequently an iron deficiency state in the liver. However, the molecular mechanism of decreased iron accumulation in the liver induced by long-term exposure to Cd is unknown. In this study, we investigated the hepatic accumulation of iron and the proximal duodenal expression of the genes involved in iron transport using mice chronically exposed to Cd. Five-week-old female C57BL/6J mice were fed a diet containing 300 ppm Cd for 12, 15, 19 and 21 months. The iron concentration in the liver was markedly decreased by Cd. Among iron-transport-related genes in the proximal duodenum, the gene expression of HCP1 and Cybrd1 was significantly decreased by Cd. HCP1 is an influx transporter of heme iron. Cybrd1 is a reductase that allows non-heme iron to enter cells. The expression of iron-transport-related genes on the duodenal basolateral membrane side was hardly altered by Cd. These results suggest that long-term exposure to Cd suppresses the expression of HCP1 and Cybrd1 in the proximal duodenum, resulting in reduced iron absorption and iron accumulation in the liver. [ABSTRACT FROM AUTHOR]

Published
2023
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9. A Novel In Vitro Assay Using Human iPSC-Derived Sensory Neurons to Evaluate the Effects of External Chemicals on Neuronal Morphology: Possible Implications in the Prediction of Abnormal Skin Sensation

Author

Satoh, Masahiko, primary, Suzuki, Tamie, additional, Sakurai, Tetsuhito, additional, Toyama, Sumika, additional, Kamata, Yayoi, additional, Kondo, Shinya, additional, Suga, Yasushi, additional, Tominaga, Mitsutoshi, additional, and Takamori, Kenji, additional

Published
2021
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11. Neurobehavioral effects of the exposure to mercury vapor and methylmercury during postnatal period on mice

Author

Lee, Jin-Yong, Yoshida, Minoru, Satoh, Masahiko, and Watanabe, Chiho

Abstract

In this study, we investigated the neurobehavioral alterations and modifications of gene expression in the brains of female mice exposed to low-level mercury vapor and/or methylmercury during postnatal development. The mice were exposed to low-level mercury vapor at a mean concentration of 0.094 mg/m3and supplied with tap water containing 5 ppm methylmercury from postnatal day 11 to 12 weeks of age. Behavioral analyses were performed at 17 weeks of age. Total locomotor activity in the open field test and the retention trial performance in the passive avoidance test were significantly reduced in the combined exposure group compared with those in the control group. The differences in locomotor activity and performance in the retention trial at 17 weeks were no longer detected at 45 weeks. These results suggest that the effect of aging on the behavioral abnormalities resulting from postnatal exposure to mercury complexes are not significant. In the microarray analysis of brains in the combined exposure group, the gene expression levels of Ano2and Sgk1were decreased. Real-time RT-PCR analysis confirmed these changes caused by combined mercury exposure, showing significant downregulation of Ano2and Sgk1in the cerebrum. These genes play key roles in the brain as a calcium-activated chloride channel and as a kinase that responds to cellular stress, respectively. Our findings provide insight into the neurobehavioral changes caused by combined mercury exposure.

Published
2023
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17. Galectin-3 enhances neutrophil motility and extravasation into the airways during Aspergillus fumigatus infection

Author

Snarr, Brendan D., primary, St-Pierre, Guillaume, additional, Ralph, Benjamin, additional, Lehoux, Mélanie, additional, Sato, Yukiko, additional, Rancourt, Ann, additional, Takazono, Takahiro, additional, Baistrocchi, Shane R., additional, Corsini, Rachel, additional, Cheng, Matthew P., additional, Sugrue, Michele, additional, Baden, Lindsey R., additional, Izumikawa, Koichi, additional, Mukae, Hiroshi, additional, Wingard, John R., additional, King, Irah L., additional, Divangahi, Maziar, additional, Satoh, Masahiko S., additional, Yipp, Bryan G., additional, Sato, Sachiko, additional, and Sheppard, Donald C., additional

Published
2020
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22. Cadmium-induced protein ubiquitination in UBA80 knockdown HK-2 cells

Author

Satoh Masahiko, Lee Jin-Yong, Hwang Gi-Wook, and Tokumoto Maki

Subjects
0301 basic medicine, 03 medical and health sciences, Gene knockdown, Cadmium, 030104 developmental biology, Chemistry, chemistry.chemical_element, Bioinformatics, Protein ubiquitination, Cell biology
Published
2016

24. Basal level of p53 regulates cell population homeostasis

Author

Rancourt, Ann, Sato, Sachiko, and Satoh, Masahiko S.

Abstract

p53 regulates a broad range of processes in cells exposed to various stresses. Although, in unstressed cells, p53 is maintained at low levels, it is unclear if these low levels of p53 have any functional roles. Thus, we investigated the roles of basal levels of p53 using a single-cell lineage tracking technique. We compared the spatiotemporal responses of p53-proficient cancer cells with cells in which p53 gene expression had been silenced. We found that the p53-proficient cell population included a subpopulation of fast-growing cells with a shorter cell-doubling time than other slow-growing cells. p53 silencing reduced the cell-doubling time of the slow-growing cells, thus converting them to faster growing cells. In contrast, the growth rate of the fast-growing cells was unaffected by basal levels of p53, suggesting that growth of slow-growing but not fast-growing cells were regulated by p53 levels. In addition, silencing p53 increased the incidences of multipolar cell division and cell death among the slow-growing cells. These results suggest that basal levels of p53 act to maintain a balance between the fast- and slow-growing cell subpopulations and to suppress the occurrence of abnormal cellular events. We therefore propose that basal levels of p53 help to control cell population homeostasis by regulating the growth and maintaining the integrity of slow-growing cells.

Published
2018
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36. Role of poly(ADP-ribose) formation in DNA repair

Author

Satoh, Masahiko S. and Lindahl, Tomas

Subjects
DNA repair -- Research, Ligases -- Research, DNA polymerases -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Published
1992

37. A cellular defense pathway regulating transcription through poly(ADP-ribosyl)ation in response to DNA damage

Author

Vispe, Stephane, Yung, Tetsu M. C., Ritchot, Janelle, Serizawa, Hiroaki, and Satoh, Masahiko S.

Subjects
DNA damage -- Research, Cell research -- Analysis, Science and technology
Abstract

DNA damage is known to trigger key cellular defense pathways such as those involved in DNA repair. Here we provide evidence for a previously unrecognized pathway regulating transcription in response to DNA damage and show that this regulation is mediated by the abundant nuclear enzyme poly(ADP-ribose) polymerase. We found that poly(ADP-ribose) polymerase reduced the rate of transcription elongation by RNA polymerase II, suggesting that poly(ADP-ribose) polymerase negatively regulates transcription, possibly through the formation of poly(ADP-ribose) polymerase-RNA complexes, in damaged cells, poly(ADP-ribose) polymerase binds to DNA breaks and automodifies itself in the presence of [NAD.sup.+], resulting in poly(ADP-ribose) polymerase inactivation. We found that automodification of poly(ADP-ribose) polymerase in response to DNA damage resulted in the up-regulation of transcription, presumably because automodified poly(ADP-ribose) polymerase molecules were released from transcripts, thereby relieving the block on transcription. Because agents that damage DNA damage RNA as well, up-regulation of RNA synthesis in response to DNA damage may provide cells with a mechanism to compensate for the loss of damaged transcripts and may be critical for cell survival after exposure to DNA-damaging agents.

Published
2000

42. Metallothionein as an Anti-Inflammatory Mediator

Author

Inoue, Ken-ichiro, Takano, Hirohisa, Shimada, Akinori, and Satoh, Masahiko

Subjects
Article Subject
Abstract

The integration of knowledge concerning the regulation of MT, a highly conserved, low molecular weight, cystein-rich metalloprotein, on its proposed functions is necessary to clarify how MT affects cellular processes. MT expression is induced/enhanced in various tissues by a number of physiological mediators. The cellular accumulation of MT depends on the availability of cellular zinc derived from the diet. MT modulates the binding and exchange/transport of heavy metals such as zinc, cadmium, or copper under physiological conditions and cytoprotection from their toxicities, and the release of gaseous mediators such as hydroxyl radicals or nitric oxide. In addition, MT reportedly affects a number of cellular processes, such as gene expression, apoptosis, proliferation, and differentiation. Given the genetic approach, the apparently healthy status of MT-deficient mice argues against an essential biological role for MT; however, this molecule may be critical in cells/tissues/organs in times of stress, since MT expression is also evoked/enhanced by various stresses. In particular, because metallothionein (MT) is induced by inflammatory stress, its roles in inflammation are implied. Also, MT expression in various organs/tissues can be enhanced by inflammatory stimuli, implicating in inflammatory diseases. In this paper, we review the role of MT of various inflammatory conditions.

Published
2009
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46. Role of metallothionein in murine experimental colitis

Author

TSUJI, TOSHIFUMI, primary, NAITO, YUJI, additional, TAKAGI, TOMOHISA, additional, KUGAI, MUNEHIRO, additional, YORIKI, HIROYUKI, additional, HORIE, RYUSUKE, additional, FUKUI, AKIFUMI, additional, MIZUSHIMA, KATSURA, additional, HIRAI, YASUKO, additional, KATADA, KAZUHIRO, additional, KAMADA, KAZUHIRO, additional, UCHIYAMA, KAZUHIKO, additional, HANDA, OSAMU, additional, KONISHI, HIDEYUKI, additional, YAGI, NOBUAKI, additional, ICHIKAWA, HIROSHI, additional, YANAGISAWA, RIE, additional, SUZUKI, JUNKO S., additional, TAKANO, HIROHISA, additional, SATOH, MASAHIKO, additional, and YOSHIKAWA, TOSHIKAZU, additional

Published
2013
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