Hypericin-photodynamic therapy inhibits angiogenesis through inhibiting proliferation, migration and lumen forming in human umbilical vein endothelial cells
Zhang Qian,Li Zhuoheng,Li Yuanyuan,Li Chenwen,Guan Haiyan,Cui Huanhuan,Li Ziwei,Lu Laichun.Hypericin-photodynamic therapy inhibits angiogenesis through inhibiting proliferation, migration and lumen forming in human umbilical vein endothelial cells[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(11):1125-1130.
Zhang Qian,Li Zhuoheng,Li Yuanyuan,Li Chenwen,Guan Haiyan,Cui Huanhuan,Li Ziwei,Lu Laichun.Hypericin-photodynamic therapy inhibits angiogenesis through inhibiting proliferation, migration and lumen forming in human umbilical vein endothelial cells[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(11):1125-1130.DOI:
Objective To determine the effect of hypericin-photodynamic therapy (HY-PDT) on the proliferation
migration and lumen forming in human umbilical vein endothelial cells (HUVECs)
and investigate the underlying mechanism of HY-PDT in anti-angiogenesis. Methods HUVECs were incubated in the culture medium containing HY or hematoporphyrin (HP
positive c
ontrol) for 24 h in the dark
and then were irradiated by a 585 nm light at a dose of 1.0 J/cm
2
. After the treatment
the cells were incubated for an additional 24 h in the dark. Cell viability was determined by MTT assay. Cell scratch test was used to determine the migration of HUVECs. Matrigel assay was implemented to detect the effect of HY-PDT on lumen forming. The mRNA expression of Smad2
and the protein levels of ERK
1/2
p-ERK
1/2
and Smad2 were detected by quantitative real-time PCR (qRT-PCR) and Western blotting
respectively. Results HY-PDT inhibited the proliferation
migration and lumen forming in HUVECs. The ratio of p-ERK
1/2
/ERK
1/2
was significantly reduced in HUVECs following HY-PDT (P0.01). Additionally
HY-PDT remarkably decreased the mRNA and protein expression levels of Smad2 (P0.01). Conclusion HY-PDT inhibits the proliferation
migration and lumen forming in HUVECs by inhibiting activation of ERK
1/2
phosphorylation and Smad2 expression at both the transcriptional and translational levels