scholarly journals Nitric Oxide Induces TIMP-1 Expression by Activating the Transforming Growth Factor β-Smad Signaling Pathway

2005 ◽  
Vol 280 (47) ◽  
pp. 39403-39416 ◽  
Author(s):  
El-Sayed Akool ◽  
Anke Doller ◽  
Roswitha Müller ◽  
Paul Gutwein ◽  
Cuiyan Xin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Smad Signaling ◽  
Smad Signaling Pathway

MiR-21 Regulates Keloid Formation by Downregulating Smad7 via the TGF-β/Smad Signaling Pathway

2019 ◽  
Vol 40 (6) ◽  
pp. 809-817 ◽  
Author(s):  
Junliang Wu ◽  
Lu Fang ◽  
Ying Cen ◽  
Yong Qing ◽  
Junjie Chen ◽  
...  
Keyword(s):  
Growth Factor ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Skin Tumor ◽  
Smad Signaling ◽  
Downstream Target ◽  
Downstream Target Gene ◽  
Smad Signaling Pathway ◽  
Keloid Formation

Abstract A keloid is a benign fibroproliferative skin tumor that results from abnormal wound healing after injury and tends to grow beyond the boundary of the original wound; the mechanism of keloid formation is still unclear. MicroRNA-21 (MiR-21) is a representative microRNA that plays a key role in a variety of fibrotic diseases via the transforming growth factor-β/Smad signaling pathway. The aim of our study was to explore the mechanism of keloid formation. First, we found that the expression of miR-21 in keloids and keloid fibroblasts was significantly upregulated by microRNA microarray and real-time polymerase chain reaction. Additionally, at the protein level, our study confirmed that the overexpression of miR-21 could promote the process of keloid fibrosis to some extent and also indicated that a low expression of miR-21 could inhibit the process of keloid fibrosis. Finally, the results proved that miR-21 could participate in the keloid fibrosis process through negative regulation of its downstream target gene Smad7 via the transforming growth factor-β/Smad signaling pathway, which provides a guiding framework for further studies and new theoretical support for keloid clinical treatment.

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