| Project/Area Number |
05680738
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Laboratory animal science
|
|---|
| Research Institution | Saga Medical School |
|---|
Principal Investigator |
MIYABARA Shinichi Saga Medical School, Fundamental Nursing Department, Professor, 医学部, 教授 (90034644)
|
|---|
| Project Period (FY) |
1993 – 1994
|
| Project Status |
Completed (Fiscal Year 1994)
|
| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1993: ¥1,500,000 (Direct Cost: ¥1,500,000)
|
|---|
| Keywords | Genomic imprinting / T^<hp> mouse / Maternal effect / Animal model / Congenital anomalies / Overgrowth |
|---|
| Research Abstract |
Prognosis and Phenotype in the progeny of T^<hp> mice which have a large deletion on chromosome 17 and different by the parental sex transmitting the deletion. In order to establish an animal model for human congenital anomalies with genomic imprinting, T^<hp> mice with the maternally transmitted deletion (T^<hp>/+mat) were studied. T^<hp>/+pat female and C57BL/6 male were crossed in this study. Body weight, crown-rump length and placental weight of T^<hp>/+mat fetuses which died untill the end of the pregnancy were significantly larger than those of normal littermates (+/+). Organ size of T^<hp>/+mat fetuses was inclined to be larger than that of normal controls. The hypertrophic heart had a markedly hypoplastic pulmonary trunk. Myocardial cells tended to be more than the normal showing cardiac hyperplasia. The results indicate that T^<hp>/+mat fetuses showed overgrowth and organ hypertrophy suggesting an animal model for human Wiedemann-Beckwith syndrome which shows genomic imprinting in relation to IGFII.Crossing between T^<hp>/+pat female and KJR male yielded viable T^<hp>/+mat mice, which had normal pulmonary trunk, after birth. This fact indicates that the hypoplastic pulmonary trunk of T^<hp>/+mat fetuses was caused by a single gene abnormality.
|
