scholarly journals Evaluation of effect of propranolol on serum vascular endothelial growth factor and tissue inhibitor of metalloproteinase-2 levels in infantile hemangioma

2020 ◽  
Vol 25 (2) ◽  
pp. 96 ◽  
Author(s):  
Anand Pandey ◽  
Abhishek Singh ◽  
Wahid Ali ◽  
Anurag Srivastava ◽  
Archika Gupta ◽  
...  
2014 ◽  
Vol 306 (6) ◽  
pp. H789-H796 ◽  
Author(s):  
Tieqiang Zhao ◽  
Wenyuan Zhao ◽  
Weixin Meng ◽  
Chang Liu ◽  
Yuanjian Chen ◽  
...  

Vascular endothelial growth factor (VEGF)-C is a key mediator of lymphangiogenesis. Our recent study shows that VEGF-C/VEGF receptors (VEGFR)-3 are significantly increased in the infarcted rat myocardium, where VEGFR-3 is expressed not only in lymph ducts but also in myofibroblasts, indicating that VEGF-C has an unrevealed role in fibrogenesis during cardiac repair. The current study is to explore the regulation and molecular mechanisms of VEGF-C in fibrogenesis. The potential regulation of VEGF-C on myofibroblast differentiation/growth/migration, collagen degradation/synthesis, and transforming growth factor (TGF)-β and ERK pathways was detected in cultured cardiac myofibroblasts. Our results showed that VEGF-C significantly increased myofibroblast proliferation, migration, and type I/III collagen production. Matrix metalloproteinase (MMP)-2 and -9 were significantly elevated in the medium of VEGF-C-treated cells, coincident with increased tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2. Furthermore, VEGF-C activated the TGF-β1 pathway and ERK phosphorylation, which was significantly suppressed by TGF-β or ERK blockade. This is the first study indicating that in addition to lymphangiogenesis, VEGF-C is also involved in fibrogenesis through stimulation of myofibroblast proliferation, migration, and collagen synthesis, via activation of the TGF-β1 and ERK pathways.


2016 ◽  
Vol 58 (11) ◽  
pp. 1130-1135 ◽  
Author(s):  
Michio Ozeki ◽  
Akifumi Nozawa ◽  
Tomohiro Hori ◽  
Kaori Kanda ◽  
Takeshi Kimura ◽  
...  

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