Abstract |
Objective The study aimed to investigate the role of high Krüppel-like factor 5 (KLF5) expression on the pathogenesis of congenital cystic adenomatoid malformation of the lungs (CCAML) in mice. Methods A mouse model of high KLF5 expression in the lungs was established. KLF5 expression and the pulmonary lumen diameter were examined by immunohistochemistry to determine a successful model. Basement membrane damage and activity of matrix metalloproteinase-9 (MMP-9) were examined. After an adenovirus carrying KLF5 gene transfection in lung adenocarcinoma (H441) was created, changes in expression and activity of MMP-9 were determined. Results In a mouse model with high KLF5 expression, the pulmonary lumen was markedly enlarged, indicating establishment of CCAML. The basement membrane was degraded, and MMP-9 activity was significantly higher in the model group compared with the control group. Moreover, mice in a cellular model after transfection also showed higher MMP-9 activity than did controls. Conclusion High KLF5 expression may play a pivotal role in the pathogenesis of CCAML, partly through regulating the activity of MMP-9.
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Authors | Xueyan Wang, Huajing Wan, Shuo Yang, Rong Zhou, Yong Liao, Fan Wang, Ximin Chen, Zhiling Wu |
Journal | The Journal of international medical research
(J Int Med Res)
Vol. 46
Issue 7
Pg. 2856-2865
(Jul 2018)
ISSN: 1473-2300 [Electronic] England |
PMID | 29896983
(Publication Type: Journal Article)
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Chemical References |
- Klf5 protein, mouse
- Kruppel-Like Transcription Factors
- Matrix Metalloproteinase 9
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Topics |
- Animals
- Cesarean Section
- Cystic Adenomatoid Malformation of Lung, Congenital
(genetics, metabolism)
- Disease Models, Animal
- Female
- Gene Expression
- Humans
- Immunohistochemistry
- Kruppel-Like Transcription Factors
(biosynthesis, genetics)
- Lung
(metabolism)
- Matrix Metalloproteinase 9
(metabolism)
- Mice
- Pregnancy
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