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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Namba, Takushi Fujimoto, Mitsuaki Ishihara, Tomoaki Mizushima, Tohru Tanaka, Ken-ichiro Katsu, Takashi Sobue, Gen Suemasu, Shintaro Nakai, Akira Adachi, Hiroaki Takeuchi, Koji |
| Description | Author Affiliation: Suemasu S ( Graduate School of Medical and Pharmaceutical Sciences, Kumamoto University, Kumamoto 862-0973, Japan.) |
| Abstract | A major clinical problem encountered with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin, is gastrointestinal complications. Both NSAID-dependent cyclooxygenase inhibition and gastric mucosal apoptosis are involved in NSAID-produced gastric lesions, and this apoptosis is mediated by the endoplasmic reticulum stress response and resulting activation of Bax. Heat shock proteins (HSPs) have been suggested to protect gastric mucosa from NSAID-induced lesions; here we have tested this idea genetically. The severity of gastric lesions produced by indomethacin was worse in mice lacking heat shock factor 1 (HSF1), a transcription factor for hsp genes, than in control mice. Indomethacin administration up-regulated the expression of gastric mucosal HSP70. Indomethacin-induced gastric lesions were ameliorated in transgenic mice expressing HSP70. After indomethacin administration, fewer apoptotic cells were observed in the gastric mucosa of transgenic mice expressing HSP70 than in wild-type mice, whereas the gastric levels of prostaglandin E(2) for the two were indistinguishable. This suggests that expression of HSP70 ameliorates indomethacin-induced gastric lesions by affecting mucosal apoptosis. Suppression of HSP70 expression in vitro stimulated indomethacin-induced apoptosis and activation of Bax but not the endoplasmic reticulum stress response. Geranylgeranylacetone induced HSP70 at gastric mucosa in an HSF1-dependent manner and suppressed the formation of indomethacin-induced gastric lesions in wild-type mice but not in HSF1-null mice. The results of this study provide direct genetic evidence that expression of HSP70 confers gastric protection against indomethacin-induced lesions by inhibiting the activation of Bax. The HSP inducing activity of geranylgeranylacetone seems to contribute to its gastroprotective activity against indomethacin. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 29 |
| Volume Number | 284 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2009-07-17 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Apoptosis Drug Effects HSP70 Heat-Shock Proteins Metabolism Indomethacin Toxicity Stomach Ulcer Animals Anti-Inflammatory Agents, Non-Steroidal Cell Line, Tumor DNA-Binding Proteins Genetics Dinoprostone Diterpenes Pharmacology Flow Cytometry Gastric Mucosa Pathology Physiology Immunoblotting Immunohistochemistry In Situ Nick-End Labeling Mice Mice, Inbred C57BL Mice, Inbred ICR Mice, Knockout Mice, Transgenic RNA, Small Interfering Reverse Transcriptase Polymerase Chain Reaction Chemically Induced Physiopathology Transcription Factors Transfection Bcl-2-Associated X Protein Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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