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.
|Number of pages||5|
|Journal||Cell and Tissue Research|
|Publication status||Published - 2014 May|
Bibliographical noteFunding Information:
Acknowledgment This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. NRF 2011–0009570). This study was supported by a grant of the Korean Health Technology R&D Project, Ministry of Health and Welfare, Republic of Korea (A110656).
All Science Journal Classification (ASJC) codes
- Pathology and Forensic Medicine
- Cell Biology