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https://doi.org/10.1016/j.ydbio.2008.09.031
Title: | Tie2Cre-mediated inactivation of plexinD1 results in congenital heart, vascular and skeletal defects | Authors: | Zhang, Ying Singh, Manvendra K Degenhardt, Karl R Lu, Min Min Bennett, Jean Yoshida, Yutaka Epstein, Jonathan A |
Keywords: | Science & Technology Life Sciences & Biomedicine Developmental Biology plexinD1 Tissue-specific gene inactivation Congenital heart Vascular Skeletal Myocardial CARDIAC NEURAL CREST ENDOTHELIAL-CELLS AXON GUIDANCE ENDOCHONDRAL OSSIFICATION TRANSGENIC MOUSE LINEAGE ANALYSIS SEMAPHORIN ANGIOGENESIS EXPRESSION RECEPTORS |
Issue Date: | 1-Jan-2009 | Publisher: | ACADEMIC PRESS INC ELSEVIER SCIENCE | Citation: | Zhang, Ying, Singh, Manvendra K, Degenhardt, Karl R, Lu, Min Min, Bennett, Jean, Yoshida, Yutaka, Epstein, Jonathan A (2009-01-01). Tie2Cre-mediated inactivation of plexinD1 results in congenital heart, vascular and skeletal defects. DEVELOPMENTAL BIOLOGY 325 (1) : 82-93. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ydbio.2008.09.031 | Abstract: | PlexinD1 is a membrane-bound receptor that mediates signals derived from class 3 secreted semaphorins. Although semaphorin signaling in axon guidance in the nervous system has been extensively studied, functions outside the nervous system including important roles in vascular patterning have also been demonstrated. Inactivation of plexinD1 leads to neo-natal lethality, structural defects of the cardiac outflow tract, peripheral vascular abnormalities, and axial skeletal morphogenesis defects. PlexinD1 is expressed by vascular endothelial cells, but additional domains of expression have also been demonstrated including in lymphocytes, osteoblasts, neural crest and the central nervous system. Hence, the cell-type specific functions of plexinD1 have remained unclear. Here, we describe the results of tissue-specific gene inactivation of plexinD1 in Tie2 expressing precursors, which recapitulates the null phenotype with respect to congenital heart, vascular, and skeletal abnormalities resulting in neonatal lethality. Interestingly, these mutants also have myocardial defects not previously reported. In addition, we demonstrate functions for plexinD1 in post-natal retinal vasculogenesis and adult angiogenesis through the use of inducible cre-mediated deletion. These results demonstrate an important role for PlexinD1 in embryonic and adult vasculature. © 2008 Elsevier Inc. All rights reserved. | Source Title: | DEVELOPMENTAL BIOLOGY | URI: | https://scholarbank.nus.edu.sg/handle/10635/201390 | ISSN: | 00121606 1095564X |
DOI: | 10.1016/j.ydbio.2008.09.031 |
Appears in Collections: | Staff Publications Elements |
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