Abstract |
Retinoic acid (RA) is a teratogen that induces a variety of craniofacial abnormalities, including branchial arch deformities and cleft palate. Platelet-derived growth factor C ( PDGF-C) is a recently identified member of the PDGF family. PDGF-C contributes to normal development of the heart, central nervous system, kidney and palatogenesis. But the roles of PDGF-C in branchial arches development and the relationship between PDGF-C and RA-induced branchial arches abnormalities are poorly understood. We examined the effects of RA on PDGF-C and its receptor PDGFR-alpha expressions. We demonstrated that administration of RA to mouse embryos resulted in dramatic losses of PDGF-C and its receptor PDGFR-alpha. Furthermore, we confirmed that blocking PDGF-C signaling by anti- PDGF-C neutralization antibody led to branchial arch malformations similar to that of RA induced, both hypoplastic branchial arches and FBA. These findings suggest the down-regulation of PDGF-C may be one of mechanisms of branchial arch abnormalities induced by RA and PDGF-C signaling is required for branchial arch morphogenesis.
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Authors | Jing Han, Li Li, Zhaofeng Zhang, Ying Xiao, Jiuxiang Lin, Yong Li |
Journal | Toxicology letters
(Toxicol Lett)
Vol. 166
Issue 3
Pg. 248-54
(Oct 25 2006)
ISSN: 0378-4274 [Print] Netherlands |
PMID | 16956736
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Lymphokines
- Platelet-Derived Growth Factor
- platelet-derived growth factor C
- Tretinoin
- RNA
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Topics |
- Animals
- Blotting, Western
- Branchial Region
(abnormalities, drug effects, growth & development)
- Down-Regulation
(drug effects)
- Embryo Culture Techniques
- Female
- Lymphokines
(biosynthesis, physiology)
- Mice
- Mice, Inbred ICR
- Microscopy, Electron, Scanning
- Morphogenesis
(drug effects)
- Platelet-Derived Growth Factor
(biosynthesis, physiology)
- RNA
(biosynthesis, genetics)
- Reverse Transcriptase Polymerase Chain Reaction
- Signal Transduction
(drug effects)
- Tretinoin
(pharmacology)
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