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Alteration of TGF-β-ALK-Smad signaling in hyperoxia-induced bronchopulmonary dysplasia model of newborn rats
DC Field | Value | Language |
---|---|---|
dc.contributor.advisor | 김한석 | - |
dc.contributor.author | 김미화 | - |
dc.date.accessioned | 2017-07-14T01:24:27Z | - |
dc.date.available | 2017-07-14T01:24:27Z | - |
dc.date.issued | 2013-08 | - |
dc.identifier.other | 000000012883 | - |
dc.identifier.uri | https://hdl.handle.net/10371/121922 | - |
dc.description | 학위논문 (박사)-- 서울대학교 대학원 : 의학과 소아과학 전공, 2013. 8. 김한석. | - |
dc.description.abstract | Background: Bronchopulmonary dysplasia (BPD) is a main chronic lung disease that commonly occurs in preterm infants. BPD is characterized by impaired alveolarization and vascularization of the developing lung. The transforming growth factor-β (TGF-β) signaling pathway is known to play an important role during lung vascular development.
Objective: To investigate whether the regulation of TGF-β-ALK-Smad signaling pathway influences the disruption of pulmonary vascular development in newborn rats using a hyperoxia-induced BPD model. Methods: Neonatal rats were continuously exposed to 21% or 85% O2 for 7 days and subsequently kept in normoxic conditions for another 14 days. Lung tissues were harvested at each time point and were evaluated for the expression of TGF-β1, ALK1, ALK5, phosphorylated Smad1/5, phosphorylated Smad2/3, VEGF and endoglin by both biochemical and immunohistological analyses. Results: Double-fluorescence immunohistochemical staining indicated that these molecules were mainly expressed in pulmonary endothelial cells. The expression of TGF-β1 and ALK5 mRNA and protein were significantly increased in the D5 hyperoxia group, while the expression of ALK1 mRNA and protein was significantly decreased. The level of phosphorylated Smad1/5 was significantly decreased in the D7 hyperoxia group, whereas the expression of phosphorylated Smad2/3 was increased. In addition, the expression of vascular endothelial growth factor (VEGF) mRNA was increased at D1, with a subsequent decrease in the D7 hyperoxia group. There was no significant difference in endoglin expression over the entire experimental period. Conclusion: Our results indicate that exposure to hyperoxia altered the balance between the TGF-β-ALK1-Smad1/5 and TGF-β-ALK5-Smad2/3 signaling pathways in pulmonary endothelial cells, which may ultimately lead to the development of BPD. | - |
dc.description.tableofcontents | Abstract………………………………………………………… ⅰ
Contents………………………………………………………… ⅲ List of tables and figures………………………………………ⅳ Introduction……………………………………………………… 1 Material and Methods………………………………………… 5 Results………………………………………………………… 13 Discussion………………………………………………………26 References………………………………………………………31 Abstract in Korean…………………………………………… 38 | - |
dc.format | application/pdf | - |
dc.format.extent | 1547586 bytes | - |
dc.format.medium | application/pdf | - |
dc.language.iso | en | - |
dc.publisher | 서울대학교 대학원 | - |
dc.subject | Angiogenesis | - |
dc.subject | endothelial cell | - |
dc.subject | VEGF | - |
dc.subject | endoglin | - |
dc.subject.ddc | 610 | - |
dc.title | Alteration of TGF-β-ALK-Smad signaling in hyperoxia-induced bronchopulmonary dysplasia model of newborn rats | - |
dc.type | Thesis | - |
dc.description.degree | Doctor | - |
dc.citation.pages | vi, 39 | - |
dc.contributor.affiliation | 의과대학 의학과 | - |
dc.date.awarded | 2013-08 | - |
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