Document Detail


Apoptosis and regulation of Bax and Bcl-X proteins during human neonatal vascular remodeling.
MedLine Citation:
PMID:  10764659     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To verify that apoptosis is one of the possible mechanisms of neonatal vascular remodeling during the transition from fetal to neonatal circulation, we assayed for apoptosis and evaluated the expression of apoptosis-regulatory proteins in umbilical vessel versus ascending aorta, ductus arteriosus (DA) versus adjacent pulmonary artery and aorta, or aorta versus its branching arteries. Twenty-two umbilical cords (UCs), 6 DAs with adjacent aortas and pulmonary arteries, and 4 aortic arches with their branching great arteries were obtained from neonates. Smooth muscle cell (SMC) apoptosis in umbilical vessels was identified in all UCs. The expressions of Bax and Bcl-X were stronger in umbilical artery than in the neonatal aorta, but Bcl-2 was weak in both arteries in immunohistochemistry. In the immunoblot analysis of UCs, the expression of the proapoptotic short isoform of Bcl-X was stronger than in other tissue, and caspase-3 was selectively activated, whereas it was not in the other components of the cardiovascular system. In contrast, the expression patterns of the FasAg and Fas ligand were similar in umbilical artery and aorta. Regulation of Bcl-2 family proteins was also observed in other vascular sites at which SMCs undergo apoptosis on hemodynamic changes during birth, such as the DA and the branching points of the great arteries from the aortic arch. Apoptosis is involved in the regression of human umbilical vessels and the DA and in the remodeling of the branching great arteries during the neonatal period, when Bcl-2 family proteins are likely to play a key role.
Authors:
H S Kim; K K Hwang; J W Seo; S Y Kim; B H Oh; M M Lee; Y B Park
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Arteriosclerosis, thrombosis, and vascular biology     Volume:  20     ISSN:  1079-5642     ISO Abbreviation:  Arterioscler. Thromb. Vasc. Biol.     Publication Date:  2000 Apr 
Date Detail:
Created Date:  2000-04-27     Completed Date:  2000-04-27     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9505803     Medline TA:  Arterioscler Thromb Vasc Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  957-63     Citation Subset:  IM    
Affiliation:
Heart Research Institute, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
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MeSH Terms
Descriptor/Qualifier:
Aorta / chemistry,  cytology
Apoptosis*
Blood Vessels / chemistry,  cytology*
Caspase 3
Caspases / metabolism
DNA Fragmentation
Ductus Arteriosus / chemistry,  cytology
Enzyme Activation
Humans
In Situ Nick-End Labeling
Infant, Newborn
Muscle, Smooth, Vascular / anatomy & histology,  cytology
Proto-Oncogene Proteins / analysis*,  physiology
Proto-Oncogene Proteins c-bcl-2 / analysis*,  physiology
Pulmonary Artery / chemistry,  cytology
Umbilical Cord / chemistry,  cytology
bcl-2-Associated X Protein
bcl-X Protein
Chemical
Reg. No./Substance:
0/BAX protein, human; 0/BCL2L1 protein, human; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2-Associated X Protein; 0/bcl-X Protein; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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