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UV-responsive intracellular signaling pathways: MAPK, p53, and their crosstalk
Matsuda, Naoki Korean Society of Photoscience 2002 Journal of Photosciences Vol.9 No.2
There are two distinct UV-responsive signaling pathways in UV-irradiated mammalian cells, i.e., the DNA damage-dependent and -independent pathways. The former occurs in nucleus and results in growth arrest and apoptosis via post-translational modification of p53. The latter is initiated by oxidative stress and/or by damages in cell membrane or cytoplasm, which activate signaling cascade through intracellular molecules including mitogen activated protein kinases (MAPK). In normal human fibroblastic cells, all of MAPK family members, extracellular signal-related kinases (ERK), c-Jun N-terminal kinases (JNK) and p38, were rapidly phosphorylated following UV-irradiation. ERK phosphorylation was suppressed by an inhibitor of receptor tyrosine kinases (RTK). As ERK usually responds to mitogenic stimuli from RTK ligands, UV-induced ERK phosphorylation may be linked to the proliferation of survived cells. In contrast, phosphorylation of JNK and p38, as well as apoptosis, were modulated by the level of UV-generated oxidative stress Therefore, JNK and p38 may take part in oxidative stress-mediated apoptosis. Phosphorylation of p53 at Ser and Thr residues are essential for stabilization and activation of p53. Among several sites reported, we confirmed phosphorylation at Ser-15 and Ser-392 after UV-irradiation. Both of these were inhibited by a phosphoinositide 3-kinase inhibitor, presumably due to the shutdown of signals from DNA damage to p53. Phosphorylation at Ser-392 was also sensitive to an antioxidant and a p38 inhibitor, suggesting that Ser-392 of p53 is one of the possible points where DNA damage-dependent and -independent apoptic signals merge. Thus, MAPK pathway links UV-induced intracellular signals to the nuclear responses and modifies DNA damage-dependent cellular outcome, resulting in the determination of cell death.
Relationship between threatened vascular plants and the human population in Japan
Naoki Hayashi,Eriko Watanabe,Hiroyuki Matsuda 한국생태학회 2012 Journal of Ecology and Environment Vol.35 No.4
Using data sets for Japan as a whole, as arranged with approximately 10 × 10 km squares (a secondary grid), we investigated the relationship between population density and the habitats of threatened vascular plants listed in the Japanese Red Data Book; depopulated areas in the present and future, areas where under-use may be serious, and those with a predominance of elderly people; and the present state of the habitats in terms of a characteristic land use pattern. Regarding the habitats of threatened vascular plants, the progress of deterioration [(NCR + NEN)/(NCR + NEN + NVU)] in depopulated areas has been confirmed, where NCR, NEN, and NVU are the numbers of species classified as critically endangered, endangered,and vulnerable, respectively. Moreover, in grid squares used by a human such as farmland, the progress of the deterioration simply increases when population density becomes low. However, for many vascular plants, they are particularly endangered in populous areas. Local populations will decrease throughout Japan with the rate of depopulation in and around large cities being relatively slow. We also propose some issues that need further study. The deterioration by human activity may be reduced. On the other hand, some vascular plants may be adversely influenced by depopulation. Additionally, we should keep a close watch on grasslands and water areas in large cities to preserve vascular plants.
Relationship between threatened vascular plants and the human population in Japan
Hayashi, Naoki,Watanabe, Eriko,Matsuda, Hiroyuki The Ecological Society of Korea 2012 Journal of Ecology and Environment Vol.35 No.4
Using data sets for Japan as a whole, as arranged with approximately $10{\times}10$ km squares (a secondary grid), we investigated the relationship between population density and the habitats of threatened vascular plants listed in the Japanese Red Data Book; depopulated areas in the present and future, areas where under-use may be serious, and those with a predominance of elderly people; and the present state of the habitats in terms of a characteristic land use pattern. Regarding the habitats of threatened vascular plants, the progress of deterioration [$(N_{CR}+N_{EN})/(N_{CR}+N_{EN}+N_{VU})$] in depopulated areas has been confirmed, where $N_{CR}$, $N_{EN}$, and $N_{VU}$ are the numbers of species classified as critically endangered, endangered, and vulnerable, respectively. Moreover, in grid squares used by a human such as farmland, the progress of the deterioration simply increases when population density becomes low. However, for many vascular plants, they are particularly endangered in populous areas. Local populations will decrease throughout Japan with the rate of depopulation in and around large cities being relatively slow. We also propose some issues that need further study. The deterioration by human activity may be reduced. On the other hand, some vascular plants may be adversely influenced by depopulation. Additionally, we should keep a close watch on grasslands and water areas in large cities to preserve vascular plants.
Similarity of Intracellular Signaling Toward Apoptosis Following UVB and UVC Irradiation
Horikawa, Miwa,Matsuda, Naoki,Yoshida, Masahiro,Okumura, Yutaka,Watanabe, Masami,Mori, Toshio Korean Society of Photoscience 2002 Journal of Photosciences Vol.9 No.2
UV irradiation activates various intracellular signaling pathways causing cell death in a DNA damage-dependent and an independent manner. As DNA photoproducts, major forms of DNA damage, are maximally formed by UV light at 260-nm, short wavelength UV (UVC) is more harmful than middle wavelength UV (UVB). However, the differences or similarities in responses of DNA damage-independent intracellular signaling molecules to UVB and UVC are not elucidated. We examined activation of signaling molecules towards apoptosis in normal human fibroblastic cells after irradiation with UVB or UVC at a dose generating the equal amount of DNA photoproducts. Both UVB and UVC induced transient phosphorylation of ERK and sustained phosphorylation of p38. Phosphorylation of p53 at Ser15 and at Ser392 residues were also observed, which were inhibited by a phosphoinositide 3-kinase inhibitor, wortmannin. In contrast, an antioxidant N-acetyl-cysteine and a p38 inhibitor SB203580 suppressed only Ser392 phosphorylation, suggesting that UV-induced oxidative stress and p38 activation were involved in the phosphorylation of this site. The apoptic signals such as mitochondrial cytochrome C release and annexin V binding were then observed. Overall, no difference was found in chronological responses of p53, MAPK, and apoptosis between UVB-irradiated and UVC-irradiated cells. These results suggested that DNA damage-independent intracellular signaling molecules similarly responded to UVB and UVC when the equal level of DNA photoproducts were generated.
Han Xiaobo,Matsuda Naoki,Ishibashi Yuto,Odawara Aoi,Takahashi Sayuri,Tooi Norie,Kinoshita Koshi,Suzuki Ikuro 한국생체재료학회 2023 생체재료학회지 Vol.27 No.00
Microelectrode array (MEA) systems are valuable for in vitro assessment of neurotoxicity and drug efficiency. However, several difficulties such as protracted functional maturation and high experimental costs hinder the use of MEA analysis requiring human induced pluripotent stem cells (hiPSCs). Neural network functional parameters are also needed for in vitro to in vivo extrapolation.In the present study, we produced a cost effective nanofiber culture platform, the SCAD device, for long-term culture of hiPSC-derived neurons and primary peripheral neurons. The notable advantage of SCAD device is convenient application on multiple MEA systems for neuron functional analysis.We showed that the SCAD device could promote functional maturation of cultured hiPSC-derived neurons, and neurons responded appropriately to convulsant agents. Furthermore, we successfully analyzed parameters for in vitro to in vivo extrapolation, i.e., low-frequency components and synaptic propagation velocity of the signal, potentially reflecting neural network functions from neurons cultured on SCAD device. Finally, we measured the axonal conduction velocity of peripheral neurons. Conclusions: Neurons cultured on SCAD devices might constitute a reliable in vitro platform to investigate neuron functions, drug efficacy and toxicity, and neuropathological mechanisms by MEA.
Plengsuriyakarn, Tullayakorn,Matsuda, Naoki,Karbwang, Juntra,Viyanant, Vithoon,Hirayama, Kenji,Na-Bangchang, Kesara Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.15
Opisthorchis viverrini (OV)-induced cholangiocarcinoma (CCA) is an important cancer in the Great Mekong region, particularly in Thailand. Limitations of treatment options and the lack of an effective diagnostic tool for early detection of CCA are major concerns for the control of this type of cancer. The aim of the study was to investigate anti-CCA activity of the ethanolic extract of Atractylodes lancea (Thunb.) DC., and the applicability of positron emission tomography-computed tomography (PET-CT) as a tool for detection and monitoring the progression of CCA in Opisthorchis viverrini (OV)/dimethylnitrosamine (DMN)-induced CCA hamsters. Male Syrian hamsters were used for toxicity tests and anti-CCA activity evaluation. Development of CCA was induced by initial feeding of 50 metacercariae of OV, followed by drinking water containing 12.5 ppm of DMN in hamsters. The ethanolic extract of A. lancea (Thunb.) DC. was administered orally for 30 days. PET-CT was performed every 4 weeks after initiation of CCA using 18F-fluorodeoxyglucose ($^{18}F-FDG$). Results from the present study suggest that the ethanolic extract of A. lancea (Thunb.) DC. rhizome exhibited promising anti-CCA activity and safety profile in the OV/DMN-induced hamster model. To successfully apply PET-CT as a tool for early detection of tumor development and progression, modification of radiolabeling approach is required to improve its specificity for CCA cells.