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Your search keyword '"Shingo Tsuji"' showing total 5 results
Start Over Author "Shingo Tsuji" Publisher american physiological society
5 results on '"Shingo Tsuji"'

1. Role of endogenous endothelin in pathogenesis of ethanol-induced gastric mucosal injury in rats

Author

Eiji Masuda, Sunao Kawano, Kouichi Nagano, Shingo Tsuji, Yoshiyuki Takei, Nobuhiko Hayashi, Masahiko Tsujii, Masahide Oshita, Tomoki Michida, Ichizo Kobayashi, Hai-Bing Peng, Hideyuki Fusamoto, and Takenobu Kamada

Subjects
Endothelin -- Research, Gastrointestinal mucosa -- Injuries, Adenosine -- Analysis, Reflectance spectroscopy -- Usage, Biological sciences
Abstract

The function of endogenous endothelin (ET)-1 and other linked mucosal microcirculatory reactions in the pathogensis of ethanol-stimulated gastric mucosal injury was determined. Alterations in the gastric mucosal ET-1 concentrations and plasma ET-1 concentrations were found in the portal vein, following the administration of intragastric ethanol. The link between alterations in ET-1 concentration, gross mucosal hemorrhagic damage and mucosal microcirculation was determined. It was concluded that alterations in endogenous ET-1, induced by EtOH, plays a vital role in the pathogenesis of EtOH-induced gastric mucosal damage by inhibiting mucosal microcirculation.

Published
1993

2. Gastrin enhances gastric mucosal integrity through cyclooxygenase-2 upregulation in rats

Author

Yutaka Sasaki, Masahiko Tsujii, Shingo Tsuji, Sunao Kawano, Masato Komori, Yoshimi Kakiuchi, Wei Hao Sun, Arata Kimura, Shigeki Higashiyama, Naoki Kawai, Masatsugu Hori, and Masakazu Yasumaru

Subjects
Male, Physiology, medicine.medical_treatment, Immunoenzyme Techniques, Rats, Sprague-Dawley, Prostaglandin E2, Gastrin, Sulfonamides, Hepatocyte Growth Factor, Stomach, digestive, oral, and skin physiology, Gastroenterology, Hydrogen-Ion Concentration, Immunohistochemistry, Isoenzymes, medicine.anatomical_structure, Gastrointestinal hormone, Intercellular Signaling Peptides and Proteins, G cell, hormones, hormone substitutes, and hormone antagonists, Heparin-binding EGF-like Growth Factor, medicine.drug, Prostaglandin E, medicine.medical_specialty, Blotting, Western, Biology, Antibodies, Dinoprostone, Downregulation and upregulation, Physiology (medical), Internal medicine, Gastrins, medicine, Animals, Cyclooxygenase Inhibitors, Stomach Ulcer, Nitrobenzenes, Cyclooxygenase 2 Inhibitors, Epidermal Growth Factor, Ethanol, Hepatology, Membrane Proteins, Rats, Endocrinology, Cyclooxygenase 2, Gastric Mucosa, Prostaglandin-Endoperoxide Synthases, Cyclooxygenase 1, biology.protein, Cyclooxygenase
Abstract

Gastrin, PGs, and growth factors have important roles in maintaining gastrointestinal mucosal integrity. Cyclooxygenases (COX-1 and COX-2) are the key enzymes involved in PG synthesis. This study aimed to clarify the mechanisms of gastric mucosal protection by gastrin. Fasted rats were administered subcutaneous gastrin 17 with or without gastrin receptor antagonist YM022 pretreatment. Heparin-binding epidermal growth factor-like growth factor (HB-EGF) and COX-2 expression were examined using Western blot analysis. Another series of experiments investigated 1) PGE2 levels in gastric mucosa, 2) the protective action of gastrin against gastric damage by acidified ethanol, 3) the effects of a specific HB-EGF-neutralizing antibody on gastrin-induced COX-2 expression, and 4) the effects of a specific COX-2 inhibitor NS-398 on PGE2 synthesis and the mucosal protection afforded by gastrin. Gastrin dose-dependently increased HB-EGF, COX-2 expression, and PGE2 levels and reduced gastric damage. However, pretreatment with YM022 dose-dependently abolished such effects of gastrin. A specific HB-EGF- neutralizing antibody and an EGF receptor inhibitor decreased gastrin-induced COX-2 expression. NS-398 blocked gastrin-induced PGE2 synthesis and mucosal protection. In conclusion, this study demonstrates that gastrin enhances gastric mucosal integrity through COX-2, which is partially mediated by HB-EGF, and PGE2 upregulation in rats.

Published
2002

3. Cyclooxygenase-2 inhibitors suppress the growth of gastric cancer xenografts via induction of apoptosis in nude mice

Author

Masahiko Tsujii, Masatsugu Hori, Edhi S. Gunawan, Yoshiyuki Takei, Kouichi Nagano, Shingo Tsuji, Hitoshi Sawaoka, and Sunao Kawano

Subjects
Programmed cell death, medicine.medical_specialty, Physiology, Indomethacin, Transplantation, Heterologous, Mice, Nude, Apoptosis, 6-Ketoprostaglandin F1 alpha, Dinoprostone, Mice, Stomach Neoplasms, Physiology (medical), Internal medicine, Tumor Cells, Cultured, medicine, Animals, Humans, Cyclooxygenase Inhibitors, Nitrobenzenes, Mice, Inbred BALB C, Sulfonamides, Hepatology, biology, Cell growth, Stomach, Gastroenterology, Cancer, medicine.disease, Microscopy, Electron, medicine.anatomical_structure, Endocrinology, Eicosanoid, Enzyme inhibitor, biology.protein, Cancer research, Female, Cyclooxygenase, Neoplasm Transplantation
Abstract

To clarify the role of mitogen-inducible cyclooxygenase (COX-2) in the development of malignant tumors, we investigated the effects of COX-2 inhibitors on the growth of gastric cancer xenografts in nude mice in vivo. MKN45 gastric cancer cells (5 × 106cells/animal) that overexpress COX-2 were inoculated subcutaneously into athymic mice. NS-398, a specific COX-2 inhibitor, or indomethacin, a nonspecific COX-2 inhibitor, was administered orally to animals every day for 20 days. These drugs reduced the tumor volume significantly. Immunohistochemistry using bromodeoxyuridine, nick end labeling, and electron microscopy showed that NS-398 induced apoptosis in cancer cells in a dose-dependent manner and inhibited cancer cell replication slightly. Indomethacin also induced apoptosis and suppressed replication of tumor cells. There was a significant negative correlation between tumor volume and apoptotic cell number within the tumor. These results are consistent with the hypothesis that COX-2 inhibitors suppress growth of gastric cancer xenografts mainly by inducing apoptosis and suppressing replication of the neoplastic cells. It follows that COX-2 plays an important role in the development of gastric cancer.

Published
1998

4. Upregulation of GRAIL is associated with remission of ulcerative colitis.

Author

Egawa, Satoshi, Iijima, Hideki, Shinzaki, Shinichiro, Nakajima, Sachiko, Jun Wang, Jumpei Kondo, Shuji Ishii, Toshiyuki Yoshio, Takanobu Irie, Tsutomu Nishida, Yoshimi Kakiuchi, Masakazu Yasumaru, Harumasa Yoshihara, Tatsuya Kanto, Masahiko Tsujii, Shingo Tsuji, and Norlo Hayashi

Subjects
ULCERATIVE colitis, ANTIGENS, T cells, UBIQUITIN, LIGASES, LYMPHOCYTES
Abstract

Abrogating tolerance against unidentified antigens is a critical step in the pathogenesis of ulcerative colitis (UC). T cell anergy, one of the main mechanisms of tolerance, has been shown to be induced by E3 ubiquitin ligases, such as gene related to anergy in lymphocytes (GRAIL), Itch, and c-Cbl in mice. However, it is not well known whether these E3 ligases play roles in human diseases. The pathophysiological role of the E3 ligases in patients with UC was investigated. At first, the expression of GRAIL, Itch, and c-Cbl in human anergic T cells was analyzed by quantitative RT-PCR and Western immunoblotting. Next, the mRNA expression of the E3 ligases was analyzed in peripheral CD4+ T cells of 20 patients with UC and 10 healthy volunteers (HV). mRNA expression was analyzed in patients with active UC before and after treatment with prednisolone and leukocytapheresis. Anergic human CD4+ T cells expressed significantly higher levels of GRAIL, Itch, and c-Cbl than nonanergic cells. GRAIL expression was significantly higher in patients with UC in remission than in patients with active disease and in HV (P < 0.01). The level of GRAIL expression was also significantly increased in patients with active disease whose clinical activity index scores improved after treatment (P < 0.05). There were no significant differences in Itch and c-Cbl expression among patients with active UC, patients with UC in remission, and HV. These data suggest that GRAIL plays an important role in maintaining remission in patients with UC. [ABSTRACT FROM AUTHOR]

Published
2008
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