The amino acid transporter and gene expresstion during healing of gastric ulcer
Project/Area Number |
14570517
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | Nihon University |
Principal Investigator |
KATO Kimitoshi Nihon University, medicine, assistant professor, 医学部, 講師 (90204461)
|
Co-Investigator(Kenkyū-buntansha) |
NEMOTO Norimichi Nihon University, medicine, professor, 医学部, 教授 (80096875)
ISHII Yukimoto Nihon University, medicine, assistant professor, 医学部, 講師 (20246870)
|
Project Period (FY) |
2002 – 2004
|
Project Status |
Completed (Fiscal Year 2004)
|
Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2003: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2002: ¥800,000 (Direct Cost: ¥800,000)
|
Keywords | amino acid transporter / LAT1 / COX / carcinoid / colon cancer / esophageal cancer / gene expression / gastric ulcer / ストレス潰瘍 / 遺伝子発現解析 / 潰瘍治癒 |
Research Abstract |
We evaluate the amino acid transport transporters and the expressions of cyclooxygenase(COX)-1 and -2, and their interactions in the healing process of peptic ulcer or mucosal injury. COX-2 immunoreactivities were increased in interstitial tissue, granulation tissue and regenerative epithelial cells at the ulcer margin in rat acetic acid-induced ulcer. After ulcer induction, rats were treated for one week with indomethacin, a COX inhibitor, ulcer healing was significantly delayed and the immunohistochemical expression of LAT1, a Na^+-independent neutral amino acid transporter was significantly higher than that in controls. These findings suggest LAT1 were PG independently expressed and to be involved in for cell growth, the ulcer repair process. We immunohistochemically studied COX-1 and -2 expressions in gastrointestinal carcinoids and their metastases (lymph node, liver). COX-2 was expressed in all gastrointestinal carcinoids as well as their metastases. The staining pattern was diffu
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se and cytoplasmic. Strong immunoreactivity was also noted in the area of the tumor displaying stronnal invasion into the submucosa. On the other hand, faint COX-1 expression was detected in only some carcinoids. The moderate to strong immunoreactivity of LAT1 was observed in carcinoids. COX-2 and LAT1 may play a more important role in tumor growth of carcinoids. The expression of LAT1 by immunostaing was observed in the rat liver metstatic nodules of colon cacner cell and the intensity of LAT1 expression was correlative to the tumor size. We conclude that LAT1 plays an important role of liver metastatic tumors and blocking agents for LAT1 will be useful for suppressing the tumor proliferation. Esophageal squamous cell carcinoma expressed LAT1 throughout the tumor. LAT1 expression in esophageal squamous cell carcinoma was significantly higher than that in non-cancerous esophageal mucosa. LAT1 expression in esophageal carcinoma increased as the depth of invasion progressed, and as the tumor size increased. The results suggest that LAT1 plays a significant role in cell proliferation, differentiation and invasion in esophageal squamous cell carcinoma. Altered gene expressions of heat shock proteins, cell cycle regulators, protooncogenes and metabolic enzymes were recognized in the stomachs of water immersion-restraint stress (WIRS) rats using a high-density oligonucleotide array. p38 mitogen-activated protein kinase, did not reportedly show gastric expression changes in response to stress. Less
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Report
(4 results)
Research Products
(16 results)