Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs

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 pulmon...
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Autor*in:	Xueyan Wang [verfasserIn] Huajing Wan [verfasserIn] Shuo Yang [verfasserIn] Rong Zhou [verfasserIn] Yong Liao [verfasserIn] Fan Wang [verfasserIn] Ximin Chen [verfasserIn] Zhiling Wu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Übergeordnetes Werk:	In: Journal of International Medical Research - SAGE Publishing, 2015, 46(2018)
Übergeordnetes Werk:	volume:46 ; year:2018

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1177/0300060518774998

Katalog-ID:	DOAJ051443139

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520			\|a 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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700	0		\|a Zhiling Wu \|e verfasserin \|4 aut
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allfields	10.1177/0300060518774998 doi (DE-627)DOAJ051443139 (DE-599)DOAJfb26c085a3c446a28b2576705498231f DE-627 ger DE-627 rakwb eng R5-920 Xueyan Wang verfasserin aut Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Medicine (General) Huajing Wan verfasserin aut Shuo Yang verfasserin aut Rong Zhou verfasserin aut Yong Liao verfasserin aut Fan Wang verfasserin aut Ximin Chen verfasserin aut Zhiling Wu verfasserin aut In Journal of International Medical Research SAGE Publishing, 2015 46(2018) (DE-627)350260621 (DE-600)2082422-1 14732300 nnns volume:46 year:2018 https://doi.org/10.1177/0300060518774998 kostenfrei https://doaj.org/article/fb26c085a3c446a28b2576705498231f kostenfrei https://doi.org/10.1177/0300060518774998 kostenfrei https://doaj.org/toc/0300-0605 Journal toc kostenfrei https://doaj.org/toc/1473-2300 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2889 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 46 2018
spelling	10.1177/0300060518774998 doi (DE-627)DOAJ051443139 (DE-599)DOAJfb26c085a3c446a28b2576705498231f DE-627 ger DE-627 rakwb eng R5-920 Xueyan Wang verfasserin aut Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Medicine (General) Huajing Wan verfasserin aut Shuo Yang verfasserin aut Rong Zhou verfasserin aut Yong Liao verfasserin aut Fan Wang verfasserin aut Ximin Chen verfasserin aut Zhiling Wu verfasserin aut In Journal of International Medical Research SAGE Publishing, 2015 46(2018) (DE-627)350260621 (DE-600)2082422-1 14732300 nnns volume:46 year:2018 https://doi.org/10.1177/0300060518774998 kostenfrei https://doaj.org/article/fb26c085a3c446a28b2576705498231f kostenfrei https://doi.org/10.1177/0300060518774998 kostenfrei https://doaj.org/toc/0300-0605 Journal toc kostenfrei https://doaj.org/toc/1473-2300 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2889 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 46 2018
allfields_unstemmed	10.1177/0300060518774998 doi (DE-627)DOAJ051443139 (DE-599)DOAJfb26c085a3c446a28b2576705498231f DE-627 ger DE-627 rakwb eng R5-920 Xueyan Wang verfasserin aut Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Medicine (General) Huajing Wan verfasserin aut Shuo Yang verfasserin aut Rong Zhou verfasserin aut Yong Liao verfasserin aut Fan Wang verfasserin aut Ximin Chen verfasserin aut Zhiling Wu verfasserin aut In Journal of International Medical Research SAGE Publishing, 2015 46(2018) (DE-627)350260621 (DE-600)2082422-1 14732300 nnns volume:46 year:2018 https://doi.org/10.1177/0300060518774998 kostenfrei https://doaj.org/article/fb26c085a3c446a28b2576705498231f kostenfrei https://doi.org/10.1177/0300060518774998 kostenfrei https://doaj.org/toc/0300-0605 Journal toc kostenfrei https://doaj.org/toc/1473-2300 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2889 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 46 2018
allfieldsGer	10.1177/0300060518774998 doi (DE-627)DOAJ051443139 (DE-599)DOAJfb26c085a3c446a28b2576705498231f DE-627 ger DE-627 rakwb eng R5-920 Xueyan Wang verfasserin aut Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Medicine (General) Huajing Wan verfasserin aut Shuo Yang verfasserin aut Rong Zhou verfasserin aut Yong Liao verfasserin aut Fan Wang verfasserin aut Ximin Chen verfasserin aut Zhiling Wu verfasserin aut In Journal of International Medical Research SAGE Publishing, 2015 46(2018) (DE-627)350260621 (DE-600)2082422-1 14732300 nnns volume:46 year:2018 https://doi.org/10.1177/0300060518774998 kostenfrei https://doaj.org/article/fb26c085a3c446a28b2576705498231f kostenfrei https://doi.org/10.1177/0300060518774998 kostenfrei https://doaj.org/toc/0300-0605 Journal toc kostenfrei https://doaj.org/toc/1473-2300 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2889 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 46 2018
allfieldsSound	10.1177/0300060518774998 doi (DE-627)DOAJ051443139 (DE-599)DOAJfb26c085a3c446a28b2576705498231f DE-627 ger DE-627 rakwb eng R5-920 Xueyan Wang verfasserin aut Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Medicine (General) Huajing Wan verfasserin aut Shuo Yang verfasserin aut Rong Zhou verfasserin aut Yong Liao verfasserin aut Fan Wang verfasserin aut Ximin Chen verfasserin aut Zhiling Wu verfasserin aut In Journal of International Medical Research SAGE Publishing, 2015 46(2018) (DE-627)350260621 (DE-600)2082422-1 14732300 nnns volume:46 year:2018 https://doi.org/10.1177/0300060518774998 kostenfrei https://doaj.org/article/fb26c085a3c446a28b2576705498231f kostenfrei https://doi.org/10.1177/0300060518774998 kostenfrei https://doaj.org/toc/0300-0605 Journal toc kostenfrei https://doaj.org/toc/1473-2300 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2889 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 46 2018
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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. 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callnumber-first	R - Medicine
author	Xueyan Wang
spellingShingle	Xueyan Wang misc R5-920 misc Medicine (General) Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs
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topic_title	R5-920 Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs
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title	Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs
ctrlnum	(DE-627)DOAJ051443139 (DE-599)DOAJfb26c085a3c446a28b2576705498231f
title_full	Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs
author_sort	Xueyan Wang
journal	Journal of International Medical Research
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author_browse	Xueyan Wang Huajing Wan Shuo Yang Rong Zhou Yong Liao Fan Wang Ximin Chen Zhiling Wu
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author-letter	Xueyan Wang
doi_str_mv	10.1177/0300060518774998
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title_sort	elevated krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs
callnumber	R5-920
title_auth	Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs
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.
abstractGer	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.
abstract_unstemmed	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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title_short	Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs
url	https://doi.org/10.1177/0300060518774998 https://doaj.org/article/fb26c085a3c446a28b2576705498231f https://doaj.org/toc/0300-0605 https://doaj.org/toc/1473-2300
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author2	Huajing Wan Shuo Yang Rong Zhou Yong Liao Fan Wang Ximin Chen Zhiling Wu
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up_date	2024-07-03T20:22:59.960Z
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Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs

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