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Downregulation of bcl - xL Is Relevant to UV - induced Apoptosis in Fibroblasts
(Yuki Nakagawa),(Seiji Okada),(Masahiko Hatano),(Masaaki Ebara),(Hiromitsu Saisho),(Takeshi Tokuhisa) 생화학분자생물학회 2002 BMB Reports Vol.35 No.5
Exposure to ultraviolet light (UV) induces apoptosis in mammalian cells. The caspase group of proteases is required for the apoptosis. This pathway is initiated by a release of cytochrome c from the mitochondria into the cytosol. Several Bcl-2 family proteins can regulate the release of cytochrome c by stabilizing the mitochondrial membrane. Here we show that expression of the endogenous bcl-xL was strongly downregulated in NIH3T3 cells within 2 h after UV-C irradiation, and that of bax was upregulated from 8 h after irradiation. Apoptosis was induced in more than 50% of the NIH3T3 cells 48 h after irradiation. Constitutive overexpression of bcl-xL in NIH3T3 cells protected the UV-induced apoptosis by preventing the loss of mitochondrial membrane potential and the activation of caspase 9. These results suggest that downregulation of Bcl-xL is relevant to UV-induced apoptosis of fibroblasts.
Downregulation of bcl-xL Is Relevant to UV-induced Apoptosis in Fibroblasts
Nakagawa, Yuki,Okada, Seiji,Hatano, Masahiko,Ebara, Masaaki,Saisho, Hiromitsu,Tokuhisa, Takeshi Korean Society for Biochemistry and Molecular Biol 2002 Journal of biochemistry and molecular biology Vol.35 No.5
Exposure to ultraviolet light (UV) induces apoptosis in mammalian cells, The caspase group of proteases is required for the appotosis. This pathway is initiated by a release of cytochrome c from the mitochondria into the cytosol. Several Bcl-2 family proteins can regulate the release of cytochrome c by stabilizing the mitochondrial membrane. Here we show that expression of the endogenous bcl-xL was strongly downregulated in NIH3T3 cells within 2 h after UV-C irradiation, and that of bax was upregulated from 8 h after irradiation. Apoptosis was induced in more than 50% of the NIH3T3 cells 48 h after irradiation. Constitutive overexpression of bcl-xL in NIH3T3 cells protected the UV-induced apoptosis by preventing the loss of mitochondrial membrane potential and the activation of caspase 9. There results suggest that downregulation of Bcl-xL is relevant to UV-induced apoptosis of tibroblasts.
Phototransduction and Visual Cycle in the Ascidian Tadpole Larva
Kusakabe, Takehiro,Nakashima, Yuki,Kusakabe, Rie,Horie, Takeo,Kawakami, Isao,Yoshida, Reiko,Inada, Kyoko,Nakagawa, Masashi,Tsuda, Motoyuki Korean Society of Photoscience 2002 Journal of Photosciences Vol.9 No.2
Ascidians are lower chordates, and their tadpole-like larvae share a basic body plan with vertebrates. To study photoreceptive systems in ascidians, we have isolated and characterized cDNA clones for three opsins, five G protein ${\alpha}$ subunits (G${\alpha}$), catalytic and regulatory subunits of cGMP phosphodiesterase (PDE), and arrestin from the ascidian Ciona intestinalis tadpole larva. Ci-opsin1 and Ci-opsin2 are vertebrate-type opsins, while Ci-opsin3 is a retinal photoisomerase similar to retinochrome and mammalian RGR. Both Ci-opsin1 and arrestin are specifically localized in the photoreceptor cells of the ocellus, whereas Ci -opsin2 is not expressed in the photoreceptors, but is co-localized in another population of neurons in the brain with PDE (Ci-PDE9 and Ci-PDE$\delta$). Ci-opsin3 is present in the entire region of the brain. Though five different cDNAs encoding Ga have been cloned, no transducin-type G protein has been found yet. Interestingly, one of G${\alpha}$i isoform is conspicuously expressed in the entire region of the brain. The Ci-opsin3 gene expression was observed in a broad area of the brain vesicle as well as in the visceral ganglion. Genes encoding ascidian homologs of CRALBP and ${\beta}$-CD, whose function is required for the mammalian visual cycle, are co-expressed with Ci-opsin3 in the brain vesicle and visceral ganglion. Localization of Ci-opsin3, CRALBP, and ${\beta}$-CD in a broad area of the brain suggests that the brain of the ascidian larva has a visual cycle system similar to that of the vertebrate RPE. Based on these data, we discuss the evolution of vertebrate visual systems.
Light induced recombination center at SiO2/Si interface by the reactive plasma deposition
Tomohiko Hara,Taichi Tanaka,Kazuhito Nakagawa,Yuki Isogai,Takefumi Kamioka,Yoshio Ohshita 대한금속·재료학회 2021 ELECTRONIC MATERIALS LETTERS Vol.17 No.5
Effect of lights with various wavelength on the defect generation in reactive plasma deposition (RPD) process is studiedusing capacitance–voltage analysis. Indium-tin oxide (ITO) deposition by RPD dramatically decreases the minority carrierlifetime and deteriorates the solar cell performances. The wavelength of light which arrives at the SiO2/Si interface andSi crystal is controlled by varying the SiO2thickness in SiO2/Si samples. Thick SiO2layer with above 10 nm prevents thepenetration of many ions into the SiO2/Si interface layer, and the only effects of light wavelength on the defect formation areobtained. When SiO2thickness are 10–600 nm, a large number of defects of the order of 1012eV−1 cm−2, mid gap energyof Si, are generated by ITO-RPD independent of SiO2thickness. These defects are expected to be recombination centers. These SiO2thicknesses are enough thick to completely absorb the light below-110-nm-wavelength. The results suggest thatthe light of longer wavelength than 110 nm mainly contributes to the defect formation in RPD process. On the other hand,in the case of 500 μm thick SiO2,the generated defects are significantly decreased by one order of magnitude (or decreasedto the order of 1010eV−1 cm−2) small amount of defect is generated. This thick SiO2prevents the penetration of light withbelow 180 nm wavelength into the Si. Therefore, the light with around 110–180 nm wavelength, which are generated by Arand/or O2plasma in RPD process, mainly forms the recombination-active defects.