@Article{ecn.2015.0360,
AUTHOR = {J. Jing, T. T. Dou, J. Q. Yang, X. B. Chen, H. L. Cao, M. Min, S. Q. Cai, M. Zheng, X. Y. Man},
TITLE = {Role of endothelin-1 in the skin fibrosis of systemic sclerosis},
JOURNAL = {European Cytokine Network},
VOLUME = {26},
YEAR = {2015},
NUMBER = {1},
PAGES = {10--14},
URL = {http://www.techscience.com/ECN/v26n1/65552},
ISSN = {1952-4005},
ABSTRACT = {Endothelin-1 (ET-1) acts as a key regulator of vasoconstriction and fibrosis. Many previous studies
have focused on the role of ET-1 in scleroderma (systemic sclerosis, SSc). We investigated the effects of ET-1 on the
production of extracellular matrix in SSc and normal skin fibroblasts. Primary cultured dermal fibroblasts from
SSc patients and healthy controls were treated with ET-1 (25 ng/mL) for 0 min, 15 min, 1 h, 24 h, 48 h and 72 h,
respectively. Our results showed that, in SSc fibroblasts, ET-1 upregulated collagen type I, connective tissue growth
factor (CTGF), type I plasminogen activator inhibitor (PAI-1) and pAkt in a time-dependent manner within 72 h; in
normal fibroblasts, 25 ng/mL ET-1 stimulation correlated with high levels of CTGF, PAI-1 and pAkt. The secretion
of fibronectin (FN), collagen type I, and PAI-1 is markedly increased in the supernatant of both SSc fibroblasts
and normal fibroblasts. Furthermore, ET-1 phosphorylates Smad2 and Smad3 in normal fibroblasts, but not in SSc
fibroblasts. In conclusion, our results demonstrated that ET-1 may induce fibrosis in dermal fibroblasts through
Akt signals.},
DOI = {10.1684/ecn.2015.0360}
}