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Your search keyword '"Nakane, Tatsuto"' showing total 10 results
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10 results on '"Nakane, Tatsuto"'

2. Enhancement of keratinocyte survival and migration elicited by interleukin 24 upregulation in dermal microvascular endothelium upon welding-fume exposure.

Author

Kono, Maori, Ishihara, Nami, Nakane, Tatsuto, Nabetani, Yu, Kajino, Mizuo, Okuda, Tomoaki, Hayashi, Masahiko, Koriyama, Chihaya, Vogel, Christoph F.A., Tsuji, Mayumi, and Ishihara, Yasuhiro

Subjects
WELDING fumes, KERATINOCYTES, ENDOTHELIAL cells, OCCUPATIONAL exposure, OXIDATIVE stress, SKIN
Abstract

Occupational exposure to welding fumes constitutes a serious health concern. Although the effects of fumes on the respiratory tract have been investigated, few apparent reports were published on their effects on the skin. The purpose of this study was to investigate the effects of exposure to welding fumes on skin cells, focusing on interleukin-24 (IL-24), a cytokine involved in the pathophysiology of skin conditions, such as atopic dermatitis and psoriasis. Treatment with welding fumes increased IL-24 expression and production levels in human dermal microvascular endothelial cells (HDMEC) which were higher than that in normal human epidermal keratinocytes. IL-24 levels in Trolox and deferoxamine markedly suppressed welding fume-induced IL-24 expression in HDMEC, indicating that oxidative stress may be involved in this cytokine expression. IL-24 released from HDMEC protected keratinocytes from welding fume-induced damage and enhanced keratinocyte migration. Serum IL-24 was higher in welding workers than in general subjects and was positively correlated with elevated serum levels of 8-hydroxy-2'-deoxyguanosine, an oxidative stress marker. In summary, welding fumes enhanced IL-24 expression in HDMEC, stimulating keratinocyte survival and migration. IL-24 expression in endothelial cells may act as an adaptive response to welding-fume exposure in the skin. [ABSTRACT FROM AUTHOR]

Published
2024
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3. Na+/Ca2+ exchanger mediates cold Ca2+ signaling conserved for temperature-compensated circadian rhythms

Author

KON, NAOHIRO, WANG, HSIN-TZU, S., KATO YOSHIAKI, UEMOTO, KYOUHEI, KAWAMOTO, NAOHIRO, KAWASAKI, KOJI, ENOKI, RYOSUKE, KUROSAWA, GEN, NAKANE, TATSUTO, SUGIYAMA, YASUNORI, TAGASHIRA, HIDEAKI, ENDO, MOTOMU, IWASAKI, HIDEO, IWAMOTO, TAKAHIRO, KUME, KAZUHIKO, FUKADA, YOSHITAKA, KON, NAOHIRO, WANG, HSIN-TZU, S., KATO YOSHIAKI, UEMOTO, KYOUHEI, KAWAMOTO, NAOHIRO, KAWASAKI, KOJI, ENOKI, RYOSUKE, KUROSAWA, GEN, NAKANE, TATSUTO, SUGIYAMA, YASUNORI, TAGASHIRA, HIDEAKI, ENDO, MOTOMU, IWASAKI, HIDEO, IWAMOTO, TAKAHIRO, KUME, KAZUHIKO, and FUKADA, YOSHITAKA

Abstract

Circadian rhythms are based on biochemical oscillations generated by clock genes/proteins, which independently evolved in animals, fungi, plants, and cyanobacteria. Temperature compensation of the oscillation speed is a common feature of the circadian clocks, but the evolutionary-conserved mechanism has been unclear. Here, we show that Na+/Ca2+ exchanger (NCX) mediates cold-responsive Ca2+ signaling important for the temperature-compensated oscillation in mammalian cells. In response to temperature decrease, NCX elevates intracellular Ca2+, which activates Ca2+/calmodulin-dependent protein kinase II and accelerates transcriptional oscillations of clock genes. The cold-responsive Ca2+ signaling is conserved among mice, Drosophila, and Arabidopsis. The mammalian cellular rhythms and Drosophila behavioral rhythms were severely attenuated by NCX inhibition, indicating essential roles of NCX in both temperature compensation and autonomous oscillation. NCX also contributes to the temperature-compensated transcriptional rhythms in cyanobacterial clock. Our results suggest that NCX-mediated Ca2+ signaling is a common mechanism underlying temperature-compensated circadian rhythms both in eukaryotes and prokaryotes.

Published
2023

4. Na+/Ca2+ exchanger mediates cold Ca2+ signaling conserved for temperature-compensated circadian rhythms

Author

KON, NAOHIRO, WANG, HSIN-TZU, S. KATO, YOSHIAKI, UEMOTO, KYOUHEI, KAWAMOTO, NAOHIRO, KAWASAKI, KOJI, ENOKI, RYOSUKE, KUROSAWA, GEN, NAKANE, TATSUTO, SUGIYAMA, YASUNORI, TAGASHIRA, HIDEAKI, ENDO, MOTOMU, IWASAKI, HIDEO, IWAMOTO, TAKAHIRO, KUME, KAZUHIKO, FUKADA, YOSHITAKA, KON, NAOHIRO, WANG, HSIN-TZU, S. KATO, YOSHIAKI, UEMOTO, KYOUHEI, KAWAMOTO, NAOHIRO, KAWASAKI, KOJI, ENOKI, RYOSUKE, KUROSAWA, GEN, NAKANE, TATSUTO, SUGIYAMA, YASUNORI, TAGASHIRA, HIDEAKI, ENDO, MOTOMU, IWASAKI, HIDEO, IWAMOTO, TAKAHIRO, KUME, KAZUHIKO, and FUKADA, YOSHITAKA

Abstract

Circadian rhythms are based on biochemical oscillations generated by clock genes/proteins, which independently evolved in animals, fungi, plants, and cyanobacteria. Temperature compensation of the oscillation speed is a common feature of the circadian clocks, but the evolutionary-conserved mechanism has been unclear. Here, we show that Na+/Ca2+ exchanger (NCX) mediates cold-responsive Ca2+ signaling important for the temperature-compensated oscillation in mammalian cells. In response to temperature decrease, NCX elevates intracellular Ca2+, which activates Ca2+/calmodulin-dependent protein kinase II and accelerates transcriptional oscillations of clock genes. The cold-responsive Ca2+ signaling is conserved among mice, Drosophila, and Arabidopsis. The mammalian cellular rhythms and Drosophila behavioral rhythms were severely attenuated by NCX inhibition, indicating essential roles of NCX in both temperature compensation and autonomous oscillation. NCX also contributes to the temperature-compensated transcriptional rhythms in cyanobacterial clock. Our results suggest that NCX-mediated Ca2+ signaling is a common mechanism underlying temperature-compensated circadian rhythms both in eukaryotes and prokaryotes., identifier:2375-2548

Published
2021

6. Na + /Ca 2+ exchanger mediates cold Ca 2+ signaling conserved for temperature-compensated circadian rhythms

Author

Kon, Naohiro, primary, Wang, Hsin-tzu, additional, Kato, Yoshiaki S., additional, Uemoto, Kyouhei, additional, Kawamoto, Naohiro, additional, Kawasaki, Koji, additional, Enoki, Ryosuke, additional, Kurosawa, Gen, additional, Nakane, Tatsuto, additional, Sugiyama, Yasunori, additional, Tagashira, Hideaki, additional, Endo, Motomu, additional, Iwasaki, Hideo, additional, Iwamoto, Takahiro, additional, Kume, Kazuhiko, additional, and Fukada, Yoshitaka, additional

Published
2021
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