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Publication : Neural crest stem cell and cardiac endothelium defects in the TrkC null mouse.

First Author  Youn YH Year  2003
Journal  Mol Cell Neurosci Volume  24
Issue  1 Pages  160-70
PubMed ID  14550777 Mgi Jnum  J:109497
Mgi Id  MGI:3629022 Doi  10.1016/s1044-7431(03)00125-8
Citation  Youn YH, et al. (2003) Neural crest stem cell and cardiac endothelium defects in the TrkC null mouse. Mol Cell Neurosci 24(1):160-70
abstractText  TrkC null mice have multiple cardiac malformations. Since neural crest cells participate in cardiac outflow tract septation, the aim of this study was to determine at the cellular level the putative neural crest defect. We have identified three types of progenitor cells: stem cells that undergo self-renewal and can generate many cell types, cells that are restricted in their developmental potentials, and cells that are committed to the smooth muscle cell lineage. In TrkC null mice, there is a greater than 50% decrease in stem cell numbers and an equivalent increase in fate-restricted cells. The outflow tract wall is thickened and the endothelial tube is disorganized. We conclude that deletion of the TrkC gene causes precocious fate restrictions of the neural crest stem cell and a defect of the outflow tract endothelium, both of which may contribute to the outflow tract malformations that occur in TrkC null mice.
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