PMID- 26839446
OWN - NLM
STAT- MEDLINE
DCOM- 20160909
LR  - 20211203
IS  - 1875-8630 (Electronic)
IS  - 0278-0240 (Print)
IS  - 0278-0240 (Linking)
VI  - 2015
DP  - 2015
TI  - Kruppel-Like Factor 4 Inhibits the Transforming Growth Factor-beta1-Promoted 
      Epithelial-to-Mesenchymal Transition via Downregulating Plasminogen Activator 
      Inhibitor-1 in Lung Epithelial Cells.
PG  - 473742
LID - 10.1155/2015/473742 [doi]
LID - 473742
AB  - Transforming growth factor-beta (TGF-beta) signaling and TGF-beta-promoted 
      epithelial-to-mesenchymal transition (EMT) have been postulated to be the common 
      pathway causing pulmonary fibrosis. However, the up- or downstreaming markers of 
      TGF-beta-induced EMT still need to be further recognized. In the present study, we 
      investigated the regulation on Kruppel-like factor 4 (KLF-4) and plasminogen 
      activator inhibitor-1 (PAI-1) by TGF-beta in the murine lung epithelial LA-4 cells 
      and then examined the regulation of both markers in the TGF-beta-induced EMT by the 
      PAI-1 knockdown or the KLF-4 overexpression. Our study indicated that TGF-beta 
      induced EMT in mouse LA-4 lung epithelial cells via reducing E-cadherin, while 
      promoting Collagen I and alpha-SMA. And PAI-1 was upregulated, whereas KLF-4 was 
      downregulated in the TGF-beta-induced EMT model in LA-4 cells. Moreover, the 
      siRNA-mediated PAI-1 knockdown inhibited the TGF-beta-induced EMT, whereas the 
      adenovirus-medicated KLF-4 overexpression markedly reduced the PAI-1 expression 
      and inhibited the TGF-beta-induced EMT in LA-4 cells. In conclusion, our study 
      confirmed the downregulation of KLF-4 in the TGF-beta-induced EMT in LA-4 cells. And 
      the KLF-4 overexpression significantly reduced the TGF-beta-induced PAI-1 and thus 
      inhibited the TGF-beta-induced EMT in mouse lung epithelial LA-4 cells. It implies 
      that KLF-4 might be a promising target for effective control of the pulmonary 
      fibrosis.
FAU - Sun, Fang
AU  - Sun F
AD  - Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan 
      430060, China.
FAU - Hu, Ke
AU  - Hu K
AD  - Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan 
      430060, China.
LA  - eng
PT  - Journal Article
DEP - 20151229
PL  - United States
TA  - Dis Markers
JT  - Disease markers
JID - 8604127
RN  - 0 (Klf4 protein, mouse)
RN  - 0 (Kruppel-Like Factor 4)
RN  - 0 (Kruppel-Like Transcription Factors)
RN  - 0 (Serpin E2)
RN  - 0 (Serpine2 protein, mouse)
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Down-Regulation
MH  - Epithelial Cells/*metabolism
MH  - *Epithelial-Mesenchymal Transition
MH  - Kruppel-Like Factor 4
MH  - Kruppel-Like Transcription Factors/genetics/*metabolism
MH  - Lung/cytology/*metabolism
MH  - Mice
MH  - Serpin E2/genetics/*metabolism
PMC - PMC4709646
EDAT- 2016/02/04 06:00
MHDA- 2016/09/10 06:00
PMCR- 2015/12/29
CRDT- 2016/02/04 06:00
PHST- 2015/08/22 00:00 [received]
PHST- 2015/11/01 00:00 [revised]
PHST- 2015/11/10 00:00 [accepted]
PHST- 2016/02/04 06:00 [entrez]
PHST- 2016/02/04 06:00 [pubmed]
PHST- 2016/09/10 06:00 [medline]
PHST- 2015/12/29 00:00 [pmc-release]
AID - 10.1155/2015/473742 [doi]
PST - ppublish
SO  - Dis Markers. 2015;2015:473742. doi: 10.1155/2015/473742. Epub 2015 Dec 29.