Apurinic/apyrimidinic endonuclease1/redox factor-1 inhibits monocyte adhesion in endothelial cells

Abstract

These data provide evidence that APE1/ref-1 in endothelial cells mitigates TNF-alpha-induced monocyte adhesion and expression of vascular cell adhesion molecules, and this anti-adhesive property of APE1/ref-1 is primarily mediated by a NOS-dependent mechanism. Furthermore, APE1/ref-1 may inhibit VCAM-1 expression by inhibiting superoxide production and p38 MAPK activation.

Cytoplasmic Localization and Redox Cysteine Residue of APE1/Ref-1 Are Associated with Its Anti-Inflammatory Activity in Cultured Endothelial Cells

“…It is well known that mitogen-activated protein kinase (MAPK)s are activated by growth factors, environmental stresses and inflammatory cytokine (Chen et al, 2001). We previously reported that the overexpression of APE1/Ref-1 using the adenoviral gene transfer system inhibits TNF-α-induced ROS production and VCAM-1 in endothelial cells (Angkeow et al, 2002;Kim et al, 2006;Lee et al, 2009). In addition, p38 MAPK activation by TNF-α was blocked by overexpression of APE1/Ref-1 resulting in inhibition of TNF-α-induced VCAM-1 in endothelial cell .…”

Overexpression of Ref-1 Inhibits Lead-induced Endothelial Cell Death via the Upregulation of Catalase

“…The enzyme is particularly important under limited glutathione content conditions, such as obtain in lead (Pb)-exposed animals (Hsu, 1981;Hunaiti et al, 1995), and plays a significant role in the development of tolerance to oxidative stress in the adaptive responses of cells (Wassmann et al, 2004 (Grosch et al, 1998;Silber et al, 2002). Conversely, overexpression of Ref-1 repair functions stimulates an increase in resistance to certain alkylating agents and oxidative stresses (Tomicic et al, 1997;Grosch et al, 1998;Kim et al, 2006;Lee et al, 2009). Ref-1 and p53 proteins are required for selenium protection from DNA damage in the human and mouse fibroblasts (Fischer et al, 2006).…”

“…Intracellular superoxide and hydrogen peroxide production were detected using the superoxide-sensitive fluorophore dihydroethidine (DHE) and the peroxide-sensitive fluorophore 2',7'-dichlorodihydrofluorescein diacetate (DCF-DA) as described previously (Angkeow et al, 2002;Kim et al, 2006). In order to detect DHE or DCF-DA fluorescence, the cells were cultivated in chamber slides (2×10 5 cells/well) (Nalge Nunc International).…”

“…Ref-1 has also been shown to suppress intracellular oxidative stress and apoptosis (Angkeow et al, 2002;Ozaki et al, 2002;Yoo et al, 2004). It was recently reported that vascular endothelial cell activation and vascular inflammation were inhibited by Ref-1 overexpression (Kim et al, 2006;Song et al, 2008;Lee et al, 2009).…”

Korean Red Ginseng Extract inhibits Tumor Necrosis Factor-alpha-induced Monocyte Adhesion in the Human Endothelial Cells

“…For quantitative adhesion assay, U937 cells were fluorescently labeled with 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxy-fluorescein acetoxymethyl ester (BCECF-AM) by incubating the cells (1×10 7 cells/ml) with 1 µmol/L BCECF-AM in RPMI-1640 medium for 30 min at 37 o C and 5% CO 2 as previously described [10][11][12] . HUVECs were seeded in 24-well plates to reach confluent monolayer and pretreated with KRGE for 24 hours in EGM-2 medium.…”