MicroRNA-143-3p inhibits hyperplastic scar formation by targeting connective tissue growth factor CTGF/CCN2 via the Akt/mTOR pathway

2016 ◽  
Vol 416 (1-2) ◽  
pp. 99-108 ◽  
Author(s):  
Shengzhi Mu ◽  
Bei Kang ◽  
Weihui Zeng ◽  
Yaowen Sun ◽  
Fan Yang
2003 ◽  
Vol 83 (11) ◽  
pp. 1615-1625 ◽  
Author(s):  
Katsuyoshi Kanemoto ◽  
Joichi Usui ◽  
Shinsuke Tomari ◽  
Hideki Yokoi ◽  
Masashi Mukoyama ◽  
...  

PM&R ◽  
2010 ◽  
Vol 2 ◽  
pp. S108-S108
Author(s):  
Cheong-Hoon Seo ◽  
Jisoo Choi ◽  
Ki-Un Jang ◽  
Juyoun Lee ◽  
Jung Hyun Moon

2009 ◽  
Vol 37 (3) ◽  
pp. 727-736 ◽  
Author(s):  
Y Chang ◽  
X-Y Wu

Transforming growth factor β1 (TGF-β1) plays an important role in corneal scar formation, mediated by connective tissue growth factor (CTGF). This study was designed to investigate the effect of c-Jun N-terminal kinase (JNK) 1 and 2 on TGF-β1-regulated CTGF gene expression and corneal scar formation in telomerase-immortalized human corneal stroma fibroblast (THSF) cells. The effects of CTGF, TGF-β1 and a JNK inhibitor (SP600125) on the proliferation of THSF cells were studied using the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Both CTGF and TGF-β1 increased THSF cell proliferation and SP600125 inhibited this effect. Immunofluorescence analysis showed that TGF-β1 stimulated the activation of JNK1/2 and induced cell migration, effects that were inhibited by SP600125. Analysis by real-time reverse transcription–polymerase chain reaction showed that the mRNA levels of the genes for CTGF, fibronectin and collagen Iα1 in wound and corneal scar formation were reduced by SP600125 pre-treatment.


Hepatology ◽  
2009 ◽  
pp. NA-NA
Author(s):  
Ieva Peredniene ◽  
Eddy van de Leur ◽  
Birgit Lahme ◽  
Monika Siluschek ◽  
Axel M. Gressner ◽  
...  

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