Please use this identifier to cite or link to this item: 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

Show full item record
Files in This Item:
There are no files associated with this item.

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.