Silencing heme oxygenase-1 gene expression in retinal pigment epithelial cells inhibits proliferation, migration and tube formation of cocultured endothelial cells

被引：12

作者：

Zhang, Wenjie ^{[1
]}

Zhang, Xiaomei ^{[1
]}

Lu, Hong ^{[1
]}

Matsukura, Makoto ^{[2
]}

Zhao, Jien ^{[3
]}

Shinohara, Makoto ^{[3
]}

机构：

[1] Harbin Med Univ, Affiliated Hosp 1, Ophthalmol Hosp, Harbin 150001, Peoples R China

[2] Sojo Univ, Fac Pharmaceut Sci, Lab Clin Pharmacol & Therapeut, Kumamoto 8600082, Japan

[3] Ashikita Inst Dev Disabil, Kumamoto 8695461, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2013年 / 434卷 / 03期

关键词：

Heme oxygenase-1; Retinal pigment epithelium; Endothelial cells; Choroidal neovascularization; Vascular endothelial growth factor; Hypoxia; MACULAR DEGENERATION; ANGIOGENESIS; NEOVASCULARIZATION; VEGF; RPE; PATHWAY; COMPLEX;

D O I：

10.1016/j.bbrc.2013.03.101

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Heme oxygenase-1 (HO-1) plays an important role in the vasculature and in the angiogenesis of tumors, wounds and other environments. Retinal pigment epithelial (RPE) cells and choroidal endothelial cells (CECs) are the main cells involved in choroidal neovascularization (CNV), a process in which hypoxia plays an important role. Our aim was to evaluate the role of human RPE-cell HO-1 in the angiogenic activities of cocultured endothelial cells under hypoxia. Small interfering RNA (siRNA) for HO-1 was transfected into human RPE cell line ARPE-19, and zinc protoporphyrin (ZnPP) was used to inhibit HO-1 activity. Knockdown of HO-1 expression and inhibition of HO-1 activity resulted in potent reduction of the expression of vascular endothelial growth factor (VEGF) under hypoxia. Furthermore, knockdown of HO-1 suppressed the proliferation, migration and tube formation of cocultured endothelial cells. These findings indicated that HO-1 might have an angiogenic effect in CNV through modulation of VEGF expression and might be a potential target for treating CNV. (C) 2013 Elsevier Inc. All rights reserved.

引用

页码：492 / 497

页数：6

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