摘要
原文 | 英語 |
---|---|
頁(從 - 到) | 231-238 |
頁數 | 8 |
期刊 | International Journal of Biochemistry and Cell Biology |
卷 | 79 |
DOIs | |
出版狀態 | 已發佈 - 十月 1 2016 |
指紋
ASJC Scopus subject areas
- Biochemistry
- Cell Biology
引用此文
Klf10 deficiency in mice exacerbates pulmonary inflammation by increasing expression of the proinflammatory molecule NPRA. / Huang, Liang Ti; Chang, Hsuen Wen; Wu, Min Ju; Lai, Yong Tzuo; Wu, Wen Chi; Yu, Winston C Y; Chang, Vincent H S.
於: International Journal of Biochemistry and Cell Biology, 卷 79, 01.10.2016, p. 231-238.研究成果: 雜誌貢獻 › 文章
}
TY - JOUR
T1 - Klf10 deficiency in mice exacerbates pulmonary inflammation by increasing expression of the proinflammatory molecule NPRA
AU - Huang, Liang Ti
AU - Chang, Hsuen Wen
AU - Wu, Min Ju
AU - Lai, Yong Tzuo
AU - Wu, Wen Chi
AU - Yu, Winston C Y
AU - Chang, Vincent H S
PY - 2016/10/1
Y1 - 2016/10/1
N2 - KLF10 is a transforming growth factor (TGF)-β/Smad downstream regulated gene. KLF10 binds to the promoter of target genes and mimics the effects of TGF-β as a transcriptional factor. In our laboratory, we noted that Klf10 deficiency in mice is associated with significant inflammation of the lungs. However, the precise mechanism of this association remains unknown. We previously identified NPRA as a target gene potentially regulated by KLF10 through direct binding; NPRA knockout have known that prevented lung inflammation in a mouse model of allergic asthma. Here, we further explored the regulatory association between KLF10 and NPRA on the basis of the aforementioned findings. Our results demonstrated that KLF10 acts as a transcriptional repressor of NPRA and that KLF10 binding reduces NPRA expression in vitro. Compared with wild-type mice, Klf10-deficient mice were more sensitive to lipopolysaccharide or ovalbumin challenge and showed more severe inflammatory histological changes in the lungs. Moreover, Klf10-deficient mice showed pulmonary neutrophil accumulation. These findings collectively reveal the precise site where KLF10 signaling affects pulmonary inflammation by attenuating NPRA expression. They also verify the importance of KLF10 and atrial natriuretic peptide/NPRA in exerting influences on chronic pulmonary disease pathogenesis.
AB - KLF10 is a transforming growth factor (TGF)-β/Smad downstream regulated gene. KLF10 binds to the promoter of target genes and mimics the effects of TGF-β as a transcriptional factor. In our laboratory, we noted that Klf10 deficiency in mice is associated with significant inflammation of the lungs. However, the precise mechanism of this association remains unknown. We previously identified NPRA as a target gene potentially regulated by KLF10 through direct binding; NPRA knockout have known that prevented lung inflammation in a mouse model of allergic asthma. Here, we further explored the regulatory association between KLF10 and NPRA on the basis of the aforementioned findings. Our results demonstrated that KLF10 acts as a transcriptional repressor of NPRA and that KLF10 binding reduces NPRA expression in vitro. Compared with wild-type mice, Klf10-deficient mice were more sensitive to lipopolysaccharide or ovalbumin challenge and showed more severe inflammatory histological changes in the lungs. Moreover, Klf10-deficient mice showed pulmonary neutrophil accumulation. These findings collectively reveal the precise site where KLF10 signaling affects pulmonary inflammation by attenuating NPRA expression. They also verify the importance of KLF10 and atrial natriuretic peptide/NPRA in exerting influences on chronic pulmonary disease pathogenesis.
KW - Atrial natriuretic peptide
KW - Inflammation
KW - Krüppel-like factor 10
KW - Natriuretic peptide receptor A
KW - Pulmonary disease
UR - http://www.scopus.com/inward/record.url?scp=84984865338&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84984865338&partnerID=8YFLogxK
U2 - 10.1016/j.biocel.2016.08.027
DO - 10.1016/j.biocel.2016.08.027
M3 - Article
C2 - 27592451
AN - SCOPUS:84984865338
VL - 79
SP - 231
EP - 238
JO - International Journal of Biochemistry and Cell Biology
JF - International Journal of Biochemistry and Cell Biology
SN - 1357-2725
ER -