Role of cytosolic phospholipase A2 gene for intestinal diseases
| Project/Area Number |
18590687
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Kyushu University |
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Principal Investigator |
MATSUMOTO Takayuki Kyushu University, Hospital, Assistant Professor (10278955)
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| Co-Investigator(Kenkyū-buntansha) |
IIDA Mitsuo Kyushu University, Medical Sciences, Professor (00127961)
ESAKI Motohiro Kyushu University, Hospital, Assistant Professor (50335957)
YADA Shinichiro Kyushu University, Hospital, Assistant Professor (00346800)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,670,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Phosnholinase A2 / adenomatous polyposis / disease modifier gene / フォスフォリパーゼ / 小腸潰瘍 / 大腸腫瘍 / アラキドン酸 |
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| Research Abstract |
Cytosolic phospholipase A2 (cPLA2a) has been shown to regulate arachidonic acid release from phospholipids of the cellular membrane. It has also been shown to contribute to the polyp formation in humans and in experimental animals. Adenomatous polyposis, a hereditary condition characterized by the development of numerous colorectal adenomas, has heterogeneity in the clinical manifestations even in an identical family pedigree. We thus aimed to elucidate whether cPLA2a is a disease modifier gene in our 73 patients with adenomatous polyposis. We analyzed seven types of single nucleotide polymorphism (SNP) in genomic DNA of the subjects by means of direct sequencing and compared the results with the clinical manifestations. Severity of colorectal adenomatosis, colorectal cance4 fundic gland polyps, gastroduodenal adenomas, congenital hypertrophy of the retinal pigment epithelium, osteomas and desmoids were the target clinical manifestations. As a result, we could show that an allele C in rs12746200 (odds ratio [O!R] 2.5, 95% confidence interval [CI] 1.27-4.48, p=0.011) and an allele G in rs12746200(OR 2.59, 95% CI 1.06-6.3,p=0.034) were the SNPs, which contributed to gastric fundic gland polyps. However, the contribution of those alleles for the gastric polyp was insignificant when infection of Helicobacter pylori was taken into account. These findings suggest that cPLA2 does not seem to be a strong disease modifier gene for adenomatous polypasis. However, it seems to be related to the proliferation of gastric mucosa via Helicobacter pylori.
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Report
(3 results)
Research Products
(22 results)
