Abstract: |
We report that Id knockout mouse embryos display multiple cardiac defects, but mid-gestation lethality is rescued by the injection of 15 wild-type embryonic stem (ES) cells into mutant blastocysts. Myocardial markers altered in Id mutant cells are restored to normal throughout the chimeric myocardium. Intraperitoneal injection of ES cells into female mice before conception also partially rescues the cardiac phenotype with no incorporation of ES cells. Insulin-like growth factor 1, a long-range secreted factor, in combination with WNT5a, a locally secreted factor, likely account for complete reversion of the cardiac phenotype. Thus, ES cells have the potential to reverse congenital defects through Id-dependent local and long-range effects in a mammalian embryo. |
Keywords: |
dna-binding proteins; proto-oncogene proteins; nonhuman; mouse; phenotype; mammalia; animals; mice; mice, knockout; animal tissue; cells, cultured; cell division; gene expression profiling; embryo; stem cell transplantation; biotechnology; wild type; animalia; transcription factors; animal embryo; gene expression regulation, developmental; injection; oligonucleotide array sequence analysis; mammal; stem cells; insulin; pregnancy; inhibitor of differentiation protein 1; somatomedin c; wnt proteins; insulin-like growth factor i; repressor proteins; wnt protein; medicine; pericardium; heart; heart muscle; myocardium; congenital heart malformation; knockout mouse; lethality; embryo loss; heart defects, congenital; cell mutant; blastocyst; embryo cell; cells; cardiology; blastocyte; nucleic acid binding protein; myocytes, cardiac; gestation period; blastocysts; maternal-fetal exchange; mutant cells; inhibitor of differentiation protein 2; female; priority journal; article; cardiac defects
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