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Silencing fibroblast growth factor 7 inhibits krypton laser‐induced choroidal neovascularization in a rat model
Author(s) -
Zhang Chao,
Han Mei,
Wu Shuai
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28652
Subject(s) - gene silencing , choroidal neovascularization , microbiology and biotechnology , fibroblast , chemistry , rat model , fibroblast growth factor , neovascularization , krypton , cancer research , angiogenesis , biology , medicine , in vitro , biochemistry , retinal , receptor , gene , xenon , organic chemistry
Choroidal neovascularization (CNV), a characteristic of age‐related macular degeneration, is an underlying cause of severe vision loss among elderly patients. Fibroblast growth factor (FGF) is suggested to exert an important role in the pathogenesis of CNV. However, the molecular mechanisms governing this event are not fully elucidated. Herein, we identified the potential role of FGF7 in CNV. To examine the roles of FGF7 in the progression of CNV, rat CNV models were established and treated with small interfering RNA (siRNA) against FGF7 or FGF7 overexpression, followed by identification of expression of FGF7 in the CNV modeled rats. Next, proliferation and migration, and in vitro tube formation of human umbilical vein endothelial cells, as well as expression of vascular endothelial growth factor (VEGF) and transforming growth factor‐beta 2 (TGF‐β2) were evaluated. CNV led to upregulated FGF7 expression. Cells in the presence of FGF7 siRNA showed suppressed proliferation, migration, and tube formation, along with downregulated VEGF and TGF‐β2 expression. Taken together, functional suppression of FGF7 inhibited the onset of CNV, ultimately highlighting a novel therapeutic target for suppressing CNV progression.