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Author Zeng, Xiao-Qing ♦ Li, Na ♦ Pan, Du-Yi ♦ Miao, Qing ♦ Ma, Gui-Fen ♦ Liu, Yi-Mei ♦ Tseng, Yu-Jen ♦ Li, Feng ♦ Xu, Li-Li ♦ Chen, Shi-Yao
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ ANGIOGENESIS ♦ CELL PROLIFERATION ♦ HUMAN POPULATIONS ♦ HYPERTENSION ♦ INHIBITION ♦ LIVER ♦ MIGRATION ♦ PHOSPHORYLATION ♦ SIGNALS ♦ TUBES
Abstract Kruppel-like factor 2 (KLF2) is a crucial anti-angiogenic factor. However, its precise role in hepatic angiogenesis induced by liver sinusoidal endothelial cells (LSECs) remain unclear. This study was aimed to evaluate the effect of KLF2 on angiogenesis of LSECs and to explore the corresponding mechanism. Cultured human LSECs were infected with different lentiviruses to overexpress or suppress KLF2 expression. The CCK-8 assay, transwell migration assay and tube formation test, were used to investigate the roles of KLF2 in the proliferation, migration and vessel tube formation of LSECs, respectively. The expression and phosphorylation of ERK1/2 were detected by western blot. We discovered that the up-regulation of KLF2 expression dramatically inhibited proliferation, migration and tube formation in treated LSECs. Correspondingly, down-regulation of KLF2 expression significantly promoted proliferation, migration and tube formation in treated LSECs. Additionally, KLF2 inhibited the phosphorylation of ERK1/2 pathway, followed by the function of KLF2 in the angiogenesis of LSECs disrupted. In conclusion, KLF2 suppressed the angiogenesis of LSECs through inhibition of cell proliferation, migration, and vessel tube formation. These functions of KLF2 may be mediated through the ERK1/2 signaling pathway. - Highlights: • Overexpression of KLF2 inhibits the proliferation and migration of LSECs. • Overexpression of KLF2 inhibits the angiogenesis of LSECs. • ERK1/2 signaling pathway involved in the anti-angiogenic process of KLF2 on LSECs.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2015-09-04
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 464
Issue Number 4


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