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-ß1, 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-β1, CCSP, pJnk, and HSP70 are dramatically downregulated by loss of Runx3 during lung wound healing. However, Smad3 is up-regulated in the Runx3 KO laser-irradiated lung region. Therefore, the lung woundhealing mechanism is inhibited in the Runx3 KO mouse, which shows abnormal lung architecture, by reduced pErk, Tgf-β1, CCSP, pJnk, and HSP70 and by induced Smad3.
Bibliographical noteFunding Information:
This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science, and Technology (R13-2003-013-05001-0). J.-M.Lee.H.-J.Kwon.H.-S.Jung(*) Division in Anatomy and Developmental Biology, Department of Oral Biology, Research Center for Orofacial Hard Tissue Regeneration, Brain Korea 21 project, Oral Science Research Center, College of Dentistry, Yonsei Center of Biotechnology, Yonsei University, 250 Seongsanno, Seodaemoon-Gu, Seoul 120-752, South Korea e-mail: email@example.com
All Science Journal Classification (ASJC) codes
- Pathology and Forensic Medicine
- Cell Biology