
pmid: 12554357
The molecular mechanisms responsible for organ-specific differences in vascular development are not well established. Animals lacking the receptor tyrosine kinase Tie1 die of hemorrhage and pulmonary edema. Furthermore, cells lacking Tie1 are excluded from blood vessels of the mature lung. These findings suggest the importance of Tie1 in the pulmonary vasculature. We quantified the organ-specific expression of Tie1 during embryonic and postnatal murine development using both quantitative real-time polymerase chain reaction (PCR) and chemiluminescence employing a tie1.lacZ reporter. In the lung, Tie1 expression increases markedly immediately prior to birth and rises further in the newborn animal, a pattern not found in other organs. Furthermore, expression of Tie1 in the lung is also unique by its persistent increase in the adult animal. This unique pattern of Tie1 gene expression in the embryonic and mature lung supports a distinct role for Tie1 in the development and function of the pulmonary vasculature.
Male, Heterozygote, Gene Expression Regulation, Developmental, Receptor Protein-Tyrosine Kinases, Mice, Inbred Strains, Mice, Transgenic, Receptors, Cell Surface, Receptor, TIE-1, Mice, Animals, Newborn, Lac Operon, Genes, Reporter, Pregnancy, Animals, Female, Endothelium, Vascular, RNA, Messenger, Oligonucleotide Probes, Lung, DNA Primers
Male, Heterozygote, Gene Expression Regulation, Developmental, Receptor Protein-Tyrosine Kinases, Mice, Inbred Strains, Mice, Transgenic, Receptors, Cell Surface, Receptor, TIE-1, Mice, Animals, Newborn, Lac Operon, Genes, Reporter, Pregnancy, Animals, Female, Endothelium, Vascular, RNA, Messenger, Oligonucleotide Probes, Lung, DNA Primers
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