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1. CDC7 inhibition induces replication stress-mediated aneuploid cells with an inflammatory phenotype sensitizing tumors to immune checkpoint blockade

Author

Morita, Tomoko Yamamori, Yu, Jie, Kashima, Yukie, Kamata, Ryo, Yamamoto, Gaku, Minamide, Tatsunori, Mashima, Chiaki, Yoshiya, Miyuki, Sakae, Yuta, Yamauchi, Toyohiro, Hakozaki, Yumi, Kageyama, Shun-ichiro, Nakamura, Akito, Lightcap, Eric, Tanaka, Kosuke, Niu, Huifeng, Kannan, Karuppiah, and Ohashi, Akihiro

Published
2023
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2. Wnt activation disturbs cell competition and causes diffuse invasion of transformed cells through NF-κB-MMP21 pathway

Author

Nakai, Kazuki, Lin, Hancheng, Yamano, Shotaro, Tanaka, Shinya, Kitamoto, Sho, Saitoh, Hitoshi, Sakuma, Kenta, Kurauchi, Junpei, Akter, Eilma, Konno, Masamitsu, Ishibashi, Kojiro, Kamata, Ryo, Ohashi, Akihiro, Koseki, Jun, Takahashi, Hirotaka, Yokoyama, Hideshi, Shiraki, Yukihiro, Enomoto, Atsushi, Abe, Sohei, Hayakawa, Yoku, Ushiku, Tetsuo, Mutoh, Michihiro, Fujita, Yasuyuki, and Kon, Shunsuke

Published
2023
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23. Adeno-associated Virus Vector-mediated Interleukin-10 Induction Prevents Vascular Inflammation in a Murine Model of Kawasaki Disease

Author

Nakamura, Jun, primary, Watanabe, Sachiko, additional, Kimura, Hiroaki, additional, Kobayashi, Motoi, additional, Karasawa, Tadayoshi, additional, Kamata, Ryo, additional, Usui-Kawanishi, Fumitake, additional, Sadatomo, Ai, additional, Mizukami, Hiroaki, additional, Nagi-Miura, Noriko, additional, Ohno, Naohito, additional, Kasahara, Tadashi, additional, Minota, Seiji, additional, and Takahashi, Masafumi, additional

Published
2018
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24. Su1185 - NLRP3 Inflammasomes Contribute to Inflammation and Regeneration in Radiation-Induced Enteritis

Author

Ito, Homare, primary, Inoue, Yoshiyuki, additional, Sadatomo, Ai, additional, Yamada, Naoya, additional, Kamata, Ryo, additional, Watanabe, Sachiko, additional, Karasawa, Tadayoshi, additional, Kimura, Hiroaki, additional, Sakuma, Yasunaru, additional, Horie, Hisanaga, additional, Hosoya, Yoshinori, additional, Kitayama, Joji, additional, Sata, Naohiro, additional, and Takahashi, Masafumi, additional

Published
2018
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25. Saturated Fatty Acids Undergo Intracellular Crystallization and Activate the NLRP3 Inflammasome in Macrophages

Author

Karasawa, Tadayoshi, primary, Kawashima, Akira, additional, Usui-Kawanishi, Fumitake, additional, Watanabe, Sachiko, additional, Kimura, Hiroaki, additional, Kamata, Ryo, additional, Shirasuna, Koumei, additional, Koyama, Yutaro, additional, Sato-Tomita, Ayana, additional, Matsuzaka, Takashi, additional, Tomoda, Hiroshi, additional, Park, Sam-Yong, additional, Shibayama, Naoya, additional, Shimano, Hitoshi, additional, Kasahara, Tadashi, additional, and Takahashi, Masafumi, additional

Published
2018
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26. Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms

Author

Bumdelger, Batmunkh, Kokubo, Hiroki, Kamata, Ryo, Fujii, Masayuki, Ishida, Mari, Ishida, Takafumi, and Yoshizumi, Masao

Subjects
Mmp9, TNF-α, cardiovascular system, Abdominal aortic aneurysm, Timp1
Abstract

Abdominal aortic aneurysm (AAA) is known to develop mainly by the increased diameter of aorta through metalloproteinases (MMPs). Although activities of MMPs are tightly regulated by the presence of tissue inhibitor of MMPs (TIMPs) and imbalances between MMPs and TIMPs may serve to fragility of arterial wall, little is known about TIMPs behavior in aneurysmal formation. Here, we utilized a murine experimental AAA model, and found that by immunohistochemical analysis, Timp1 as and Timp1 mRNA levels was also revealed in aortic tissue in AAA by RT-PCR. In cultured vascular smooth muscle cells (SMCs), Tumor Necrosis Factor (TNF)-α significantly activated both Mmp9 and Timp1 expression, and they were blocked by Jun kinase inhibitor (SP600125) in a dose-dependent manner. Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kB), significantly inhibited the TNF-α-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9. Taken together, inflammatory cytokines, including TNF-α, may simultaneously induce MMPs and TIMPs for the remodeling of the medial layer, leading to the increased diameter of the aorta, the aneurysm.

Published
2013

30. Osteoprotegerin Prevents Development of Abdominal Aortic Aneurysms

Author

Bumdelger, Batmunkh, primary, Kokubo, Hiroki, additional, Kamata, Ryo, additional, Fujii, Masayuki, additional, Yoshimura, Koichi, additional, Aoki, Hiroki, additional, Orita, Yuichi, additional, Ishida, Takafumi, additional, Ohtaki, Megu, additional, Nagao, Masataka, additional, Ishida, Mari, additional, and Yoshizumi, Masao, additional

Published
2016
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37. Reverse Reaction of Lysophosphatidylinositol Acyltransferase

Author

Yamashita, Atsushi, primary, Watanabe, Masanobu, additional, Sato, Kazuaki, additional, Miyashita, Tomoyuki, additional, Nagatsuka, Tomonari, additional, Kondo, Hironori, additional, Kawagishi, Norikazu, additional, Nakanishi, Hiroki, additional, Kamata, Ryo, additional, Sugiura, Takayuki, additional, and Waku, Keizo, additional

Published
2003
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47. Cigarette smoke extract induces ferroptosis in vascular smooth muscle cells.

Author

Sampilvanjil A, Karasawa T, Yamada N, Komada T, Higashi T, Baatarjav C, Watanabe S, Kamata R, Ohno N, and Takahashi M

Subjects
Animals, Cell Death drug effects, Cell Line, Cyclohexylamines pharmacology, Deferoxamine pharmacology, Endothelial Cells drug effects, Endothelial Cells metabolism, Male, Matrix Metalloproteinase 2 metabolism, Matrix Metalloproteinase 9 metabolism, Myocytes, Smooth Muscle drug effects, NADPH Oxidases metabolism, Phenylenediamines pharmacology, Quinoxalines pharmacology, Rats, Rats, Sprague-Dawley, Siderophores pharmacology, Spiro Compounds pharmacology, Tissue Inhibitor of Metalloproteinase-1 metabolism, Ferroptosis drug effects, Muscle, Smooth, Vascular metabolism, Myocytes, Smooth Muscle metabolism, Smoke
Abstract

Cigarette smoking is a major risk factor for aortic aneurysm and dissection; however, no causative link between smoking and these aortic disorders has been proven. In the present study, we investigated the mechanism by which cigarette smoke affects vascular wall cells and found that cigarette smoke extract (CSE) induced a novel form of regulated cell death termed ferroptosis in vascular smooth muscle cells (VSMCs). CSE markedly induced cell death in A7r5 cells and primary rat VSMCs, but not in endothelial cells, which was completely inhibited by specific ferroptosis inhibitors [ferrostatin-1 (Fer-1) and Liproxstatin-1] and an iron chelator (deferoxamine). CSE-induced VSMC death was partially inhibited by a GSH precursor ( N -acetyl cysteine) and an NADPH oxidase inhibitor [diphenyleneiodonium chloride (DPI)], but not by inhibitors of pan-caspases (Z-VAD), caspase-1 (Z-YVAD), or necroptosis (necrostatin-1). CSE also upregulated IL-1β, IL-6, TNF-α, matrix metalloproteinase (MMP)-2, MMP-9, and TIMP-1 (tissue inhibitor of metalloproteinase)in A7r5 cells, which was inhibited by Fer-1. Furthermore, CSE induced the upregulation of Ptgs2 mRNA, lipid peroxidation, and intracellular GSH depletion, which are key features of ferroptosis. VSMC ferroptosis was induced by acrolein and methyl vinyl ketone, major constituents of CSE. Furthermore, CSE caused medial VSMC loss in ex vivo aortas. Electron microscopy analysis showed mitochondrial damage and fragmentation in medial VSMCs of CSE-treated aortas. All of these manifestations were partially restored by Fer-1. These findings demonstrate that ferroptosis is responsible for CSE-induced VSMC death and suggest that ferroptosis is a potential therapeutic target for preventing aortic aneurysm and dissection. NEW & NOTEWORTHY Cigarette smoke extract (CSE)-induced cell death in rat vascular smooth muscle cells (VSMCs) was completely inhibited by specific ferroptosis inhibitors and an iron chelator. CSE also induced the upregulation of Ptgs2 mRNA, lipid peroxidation, and intracellular GSH depletion, which are key features of ferroptosis. CSE caused medial VSMC loss in ex vivo aortas. These findings demonstrate that ferroptosis is responsible for CSE-induced VSMC death.

Published
2020
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48. Effects of transovarian exposure to p,p'-DDT and p,p'-DDE on avian reproduction using Japanese quails.

Author

Kamata R, Shiraishi F, Takahashi S, Shimizu A, Nakajima D, Kageyama S, Sasaki T, and Temma K

Subjects
Animals, Aryl Hydrocarbon Receptor Nuclear Translocator metabolism, Cholesterol Side-Chain Cleavage Enzyme genetics, Dose-Response Relationship, Drug, Embryo, Nonmammalian physiology, Embryonic Development drug effects, Female, Liver metabolism, Ovary enzymology, Oviducts drug effects, Ovum physiology, Receptors, Aryl Hydrocarbon metabolism, Transcription, Genetic drug effects, Coturnix physiology, DDT adverse effects, Dichlorodiphenyl Dichloroethylene adverse effects, Embryo, Nonmammalian drug effects, Ovum drug effects, Reproduction drug effects
Abstract

In the 1950s to 1970s developed countries reported declines in populations of raptorial and fish-eating birds and dichlorodiphenyltrichloroethane (DDT) and its metabolites were considered causative substances because they accumulated significantly in the tissues of wild birds and animals. However, except for the estrogenic effects of o,p'-DDT, a minor component of commercial DDT, there has been no compelling evidence that DDT directly affects avian reproductive systems. To assess the possible impact of DDT on development and reproduction of birds, exposure experiments to the major component of commercial DDT, p,p'-DDT, and its persistent metabolite, p,p'-dichlorodiphenyldichloroethylene (DDE), were performed using Japanese quail (Coturnix japonica) eggs; the test substances (3 to 100 μg/g) were injected into the yolk prior to incubation, and hatched chicks were raised to adulthood. p,p'-DDT had no significant effects on the morphology and function of the reproductive systems, although the hatchability of treated eggs was reduced at the highest dose (100 μg/g). High doses of p,p'-DDE slightly enhanced the eggshell forming ability of female quails; eggshell mass and thickness were increased at 30 μg/g or more although no morphological changes were observed in the oviduct. Transcriptions of the CYP11A1 gene in the ovaries, and of AHR and ARNT in the livers, of adult females were significantly increased at 3 μg/g or more of p,p'-DDT. Except for low hatchability, transovarian exposure to p,p'-DDT or p,p'-DDE did not markedly impair the avian reproductive systems, but the hormonal actions of these compounds are likely to change reproductive and hepatic functions even after maturation.

Published
2013
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