Lung tissue regeneration after induced injury in Runx3 KO mice

Jong Min Lee; Hyuk Jae Kwon; Suk Chul Bae; Han Sung Jung

doi:10.1007/s00441-010-1011-7

Lung tissue regeneration after induced injury in Runx3 KO mice

Jong Min Lee, Hyuk Jae Kwon, Suk Chul Bae, Han Sung Jung

Department of Oral Biology

Research output: Contribution to journal › Article › peer-review

5 Citations (Scopus)

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-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.

Original language	English
Pages (from-to)	465-470
Number of pages	6
Journal	Cell and Tissue Research
Volume	341
Issue number	3
DOIs	https://doi.org/10.1007/s00441-010-1011-7
Publication status	Published - 2010 Sept

Bibliographical note

Funding 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: hsjung@yuhs.ac

All Science Journal Classification (ASJC) codes

Pathology and Forensic Medicine
Histology
Cell Biology

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10.1007/s00441-010-1011-7

Cite this

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title = "Lung tissue regeneration after induced injury in Runx3 KO mice",

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-{\ss}1, 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.",

author = "Lee, {Jong Min} and Kwon, {Hyuk Jae} and Bae, {Suk Chul} and Jung, {Han Sung}",

note = "Funding 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: hsjung@yuhs.ac",

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AU - Kwon, Hyuk Jae

AU - Bae, Suk Chul

AU - Jung, Han Sung

N1 - Funding 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: hsjung@yuhs.ac

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N2 - 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.

AB - 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.

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Lung tissue regeneration after induced injury in Runx3 KO mice

Abstract

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