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Requirement of Runx3 in pulmonary vasculogenesis

Authors
 Jong-Min Lee  ;  Hyuk-Jae Kwon  ;  Wing-Fu Lai  ;  Han-Sung Jung 
Citation
 CELL AND TISSUE RESEARCH, Vol.356(2) : 445-449, 2014 
Journal Title
CELL AND TISSUE RESEARCH
ISSN
 0302-766X 
Issue Date
2014
MeSH
Animals ; Butadienes/pharmacology ; Core Binding Factor Alpha 3 Subunit/genetics* ; Enzyme Inhibitors/pharmacology ; Extracellular Signal-Regulated MAP Kinases/biosynthesis ; Hyperplasia/genetics ; Lung/blood supply* ; Lung/embryology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors ; Neovascularization, Physiologic/genetics ; Nitriles/pharmacology ; Platelet Endothelial Cell Adhesion Molecule-1/biosynthesis* ; Platelet Endothelial Cell Adhesion Molecule-1/metabolism ; Vascular Endothelial Growth Factor A/biosynthesis* ; Vascular Endothelial Growth Factor A/metabolism ; von Willebrand Factor/biosynthesis* ; von Willebrand Factor/metabolism
Keywords
Runx3 ; Lung development ; Vasculogenesis ; Angiogenesis ; Erk signaling
Abstract
Runx3 is essential for normal vertebrate lung development and Runx3 knockout (KO) mice die within 24 h after birth because of various organ defects including defects in alveolar expansion. For proper early lung development, vasculogenesis and angiogenesis are necessary in humans. Previous studies have reported that various signaling molecules, such as CD31, VEGF and vWF, are closely related to lung vasculogenesis and angiogenesis. To confirm the relationship between Runx3-related lung defects and vasculogenesis, the localization of various blood vessel markers is examined in WT and Runx3 KO mouse lungs at PN1. Our results indicate that CD31, VEGF and vWF were dramatically up-regulated by a loss of Runx3 during lung development. Moreover, U0126, a MEK inhibitor, rescued the lung phenotype and vascularization by regulation of ERK signaling. Therefore, it was concluded that lung vasculogenesis and angiogenesis were induced in the Runx3 KO mouse, which shows lung defects, by increased CD31, VEGF and vWF.
Full Text
http://link.springer.com/article/10.1007%2Fs00441-014-1816-x
DOI
10.1007/s00441-014-1816-x
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Others (기타) > 1. Journal Papers
Yonsei Authors
Kwon, Hyuk Jae(권혁제)
Lai, Wing Fu(여영부)
Lee, Jong Min(이종민) ORCID logo https://orcid.org/0000-0002-9466-7644
Jung, Han Sung(정한성) ORCID logo https://orcid.org/0000-0003-2795-531X
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/98659
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