期刊
APOPTOSIS
卷 14, 期 12, 页码 1472-1483出版社
SPRINGER
DOI: 10.1007/s10495-009-0338-6
关键词
Diabetic pregnancy; Congenital defects; Neural tube defect; Cardiac outflow tract defect; Apoptosis; Oxidative stress; Pax3; p53
资金
- NIH [RO1 DK52865, RO1 DK58300]
- American Diabetes Association
- Juvenile Diabetes Research Foundation
Birth defects resulting from diabetic pregnancy are associated with apoptosis of a critical mass of progenitor cells early during the formation of the affected organ(s). Insufficient expression of genes that regulate viability of the progenitor cells is responsible for the apoptosis. In particular, maternal diabetes inhibits expression of a gene, Pax3, that encodes a transcription factor which is expressed in neural crest and neuroepithelial cells. As a result of insufficient Pax3, cardiac neural crest and neuroepithelial cells undergo apoptosis by a process dependent on the p53 tumor suppressor protein. This, then provides a cellular explanation for the cardiac outflow tract and neural tube and defects induced by diabetic pregnancy.
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