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Lung tissue regeneration after induced injury in Runx3 KO mice

Authors
 Jong-Min Lee  ;  Hyuk-Jae Kwon  ;  Suk-Chul Bae  ;  Han-Sung Jung 
Citation
 CELL AND TISSUE RESEARCH, Vol.341(3) : 465-470, 2010 
Journal Title
CELL AND TISSUE RESEARCH
ISSN
 0302-766X 
Issue Date
2010
MeSH
Animals ; Cells, Cultured ; Core Binding Factor Alpha 3 Subunit/genetics* ; Lasers ; Lung/metabolism ; Lung/pathology ; Lung/physiology* ; Lung/radiation effects ; Lung Injury/genetics ; Lung Injury/pathology ; Lung Injury/physiopathology ; Lung Injury/rehabilitation* ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Biological ; Organ Culture Techniques ; Radiation Injuries, Experimental/pathology ; Radiation Injuries, Experimental/physiopathology ; Radiation Injuries, Experimental/rehabilitation ; Regeneration/genetics ; Regeneration/physiology* ; Signal Transduction/genetics ; Smad3 Protein/genetics ; Smad3 Protein/metabolism ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta1/genetics ; Transforming Growth Factor beta1/metabolism ; Wound Healing/genetics ; Wound Healing/physiology
Keywords
Runx3 KO ; Wound healing ; PErk ; Tgf-β1 ; CCSP ; PJnk ; Smad3 ; HSP70 ; Mouse (Runx3 knockout)
Abstract
Runx3 is essential for normal murine lung development, and Runx3 knockout (KO) mice, which die soon after birth, exhibit alveolar hyperplasia. Wound healing, tissue repair, and regeneration mechanisms are necessary in humans for proper early lung development. Previous studies have reported that various signaling molecules, such as pErk, Tgf-beta1, CCSP, pJnk, Smad3, and HSP70 are closely related to wound healing. In order to confirm the relationship between lung defects caused by the loss of function of Runx3 and wound healing, we have localized various wound-healing markers after laser irradiation in wild-type and in Runx3 KO mouse lungs at post-natal day 1. Our results indicate that pERK, Tgf-beta1, CCSP, pJnk, and HSP70 are dramatically down-regulated by loss of Runx3 during lung wound healing. However, Smad3 is up-regulated in the Runx3 KO laser-irradiated lung region. Therefore, the lung wound-healing mechanism is inhibited in the Runx3 KO mouse, which shows abnormal lung architecture, by reduced pErk, Tgf-beta1, CCSP, pJnk, and HSP70 and by induced Smad3.
Full Text
http://link.springer.com/article/10.1007%2Fs00441-010-1011-7
DOI
10.1007/s00441-010-1011-7
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)
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/22282913/101620
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