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Defective ALK5 signaling in the neural crest leads to increased postmigratory neural crest cell apoptosis and severe outflow tract defects

Wang, Jikui ; Nagy, Andre ; Larsson, Jonas LU ; Dudas, Marek ; Sucov, Henry M and Kaartinen, Vesa (2006) In BMC Developmental Biology 6(51).
Abstract
Background: Congenital cardiovascular diseases are the most common form of birth defects in humans. A substantial portion of these defects has been associated with inappropriate induction, migration, differentiation and patterning of pluripotent cardiac neural crest stem cells. While TGF-beta superfamily signaling has been strongly implicated in neural crest cell development, the detailed molecular signaling mechanisms in vivo are still poorly understood. Results: We deleted the TGF-beta type I receptor Alk5 specifically in the mouse neural crest cell lineage. Failure in signaling via ALK5 leads to severe cardiovascular and pharyngeal defects, including inappropriate remodeling of pharyngeal arch arteries, abnormal aortic sac development,... (More)
Background: Congenital cardiovascular diseases are the most common form of birth defects in humans. A substantial portion of these defects has been associated with inappropriate induction, migration, differentiation and patterning of pluripotent cardiac neural crest stem cells. While TGF-beta superfamily signaling has been strongly implicated in neural crest cell development, the detailed molecular signaling mechanisms in vivo are still poorly understood. Results: We deleted the TGF-beta type I receptor Alk5 specifically in the mouse neural crest cell lineage. Failure in signaling via ALK5 leads to severe cardiovascular and pharyngeal defects, including inappropriate remodeling of pharyngeal arch arteries, abnormal aortic sac development, failure in pharyngeal organ migration and persistent truncus arteriosus. While ALK5 is not required for neural crest cell migration, our results demonstrate that it plays an important role in the survival of post-migratory cardiac neural crest cells. Conclusion: Our results demonstrate that ALK5-mediated signaling in neural crest cells plays an essential cell-autonomous role in the pharyngeal and cardiac outflow tract development. (Less)
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author
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
BMC Developmental Biology
volume
6
issue
51
publisher
BioMed Central (BMC)
external identifiers
  • wos:000242017800001
  • scopus:33750825092
ISSN
1471-213X
DOI
10.1186/1471-213X-6-51
language
English
LU publication?
yes
id
3268e26f-eee4-4776-b231-eb3a01f3235f (old id 377239)
date added to LUP
2016-04-01 16:04:58
date last changed
2020-12-22 01:42:44
@article{3268e26f-eee4-4776-b231-eb3a01f3235f,
  abstract     = {Background: Congenital cardiovascular diseases are the most common form of birth defects in humans. A substantial portion of these defects has been associated with inappropriate induction, migration, differentiation and patterning of pluripotent cardiac neural crest stem cells. While TGF-beta superfamily signaling has been strongly implicated in neural crest cell development, the detailed molecular signaling mechanisms in vivo are still poorly understood. Results: We deleted the TGF-beta type I receptor Alk5 specifically in the mouse neural crest cell lineage. Failure in signaling via ALK5 leads to severe cardiovascular and pharyngeal defects, including inappropriate remodeling of pharyngeal arch arteries, abnormal aortic sac development, failure in pharyngeal organ migration and persistent truncus arteriosus. While ALK5 is not required for neural crest cell migration, our results demonstrate that it plays an important role in the survival of post-migratory cardiac neural crest cells. Conclusion: Our results demonstrate that ALK5-mediated signaling in neural crest cells plays an essential cell-autonomous role in the pharyngeal and cardiac outflow tract development.},
  author       = {Wang, Jikui and Nagy, Andre and Larsson, Jonas and Dudas, Marek and Sucov, Henry M and Kaartinen, Vesa},
  issn         = {1471-213X},
  language     = {eng},
  number       = {51},
  publisher    = {BioMed Central (BMC)},
  series       = {BMC Developmental Biology},
  title        = {Defective ALK5 signaling in the neural crest leads to increased postmigratory neural crest cell apoptosis and severe outflow tract defects},
  url          = {http://dx.doi.org/10.1186/1471-213X-6-51},
  doi          = {10.1186/1471-213X-6-51},
  volume       = {6},
  year         = {2006},
}