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CLC number: R34

On-line Access: 2017-11-06

Received: 2017-01-25

Revision Accepted: 2017-05-07

Crosschecked: 2017-10-20

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Citations:  Bibtex RefMan EndNote GB/T7714


Hai-tao Ren


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Journal of Zhejiang University SCIENCE B 2017 Vol.18 No.11 P.994-1001


Endostatin inhibits fibrosis by modulating the PDGFR/ERK signal pathway: an in vitro study

Author(s):  Yuan Li, Hai-tao Ren

Affiliation(s):  Department of Ultrasound, Women’s Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China; more

Corresponding email(s):   docliyuan@zju.edu.cn, rht@zju.edu.cn

Key Words:  Endostatin, Hypertrophic scar, Phosphorylated platelet-derived growth factor receptor (p-PDGFR), Extracellular signal-regulated kinase (ERK), Signal pathway

Yuan Li, Hai-tao Ren. Endostatin inhibits fibrosis by modulating the PDGFR/ERK signal pathway: an in vitro study[J]. Journal of Zhejiang University Science B, 2017, 18(11): 994-1001.

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author="Yuan Li, Hai-tao Ren",
journal="Journal of Zhejiang University Science B",
publisher="Zhejiang University Press & Springer",

%0 Journal Article
%T Endostatin inhibits fibrosis by modulating the PDGFR/ERK signal pathway: an in vitro study
%A Yuan Li
%A Hai-tao Ren
%J Journal of Zhejiang University SCIENCE B
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%N 11
%P 994-1001
%@ 1673-1581
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%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1700052

T1 - Endostatin inhibits fibrosis by modulating the PDGFR/ERK signal pathway: an in vitro study
A1 - Yuan Li
A1 - Hai-tao Ren
J0 - Journal of Zhejiang University Science B
VL - 18
IS - 11
SP - 994
EP - 1001
%@ 1673-1581
Y1 - 2017
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1700052

Accumulating evidence indicates that endostatin inhibits fibrosis. However, the mechanism is yet to be clarified. The aim of this study is to evaluate the effect of endostatin on platelet-derived growth factor-BB (PDGF-BB)- or transforming growth factor β1 (TGF-β1)-induced fibrosis in cultured human skin fibroblasts, and to further examine the molecular mechanisms involved. Human dermal fibroblasts were cultured in Dulbecco’s modified Eagle’s medium (DMEM) and serum-starved for 48 h before treatment. Cells were grouped as follows: “PDGF-BB”, “PDGF-BB+ endostatin”, “TGF-β1”, “TGF-β1+endostatin”, “endostatin”, and “blank control”. The fibroblasts were stimulated with either TGF-β1 or PDGF-BB for 72 h in order to set up the fibrosis model in vitro. The cells were co-cultured with either TGF-β1 or PDGF-BB and endostatin and were used to check the inhibiting effect of endostatin. A blank control group and an endostatin group were used as negative control groups. The biomarkers of fibrosis, including the expression of collagen I, hydroxyproline, and α-smooth muscle actin (α-SMA), were evaluated using an enzyme-linked immunosorbent assay (ELISA) and Western blot. The expression of phosphorylated PDGF receptor β (p-PDGFRβ), PDGFRβ, phosphorylated extracellular signal-regulated kinase (p-ERK), and ERK was detected using Western blot and immunofluorescent staining was used to explore the mechanisms. Both PDGF-BB and TGF-β1 significantly up-regulated the expression of collagen I, hydroxyproline, and α-SMA. endostatin significantly attenuated both the PDGF-BB- and TGF-β1-induced over-expression of collagen I, hydroxyproline, and α-SMA. PDGF-BB and TGF-β1 both promoted the expression of PDGFR, ERK, and p-ERK. endostatin inhibited the expression of PDGFR and p-ERK but did not affect the expression of total ERK. endostatin inhibited hypertrophic scar by modulating the PDGFRβ/ERK pathway. endostatin could be a promising multi-target drug in future fibrosis therapy.




Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


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