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ȣ - 500146 117 |
| Different Role of NF-κB Inhibitor, BAY11-7082, on TNF-α-Stimulated Vascular Smooth Muscle Cells and Endothelial Cells |
| 전남대병원 심장센터 |
| 김용숙, 안영근, 홍문화, 김계훈, 박형욱, 홍영준, 김주한, 정명호, 조정관, 박종춘, 강정채 |
Background: NF-κB, a critical transcriptional factor, plays various roles in cellular stress-induced responses in dependent on cell types. We examined the effect of BAY 11-7082, an inhibitor of NF-κB, on vascular smooth muscle cells (VSMC) and human umbilical vein endothelial cells (HUVEC). Methods: VSMC and HUVEC were stimulated with TNF-α (10ng/mL) in the presence or absence of BAY 11-7082. Proliferation, cytotoxicity, and expression of cytokines were determined by MTT assay, reverse transcriptase-polymerase chain reaction (RT-PCR), and Western blot. Results: BAY 11-7082 inhibited the VSMC proliferation in dose-dependent manner, while had no effect on HUVEC upto 10 μM. TNF-α-stimulated-VSMC and -HUVEC increased the expression of interleukin (IL)-6, IL-8, and vascular cell adhesion molecule (VCAM)-1. U937 monocyte adhesion to HUVEC was also increased by TNF-α. Pretreatment of 2μM BAY 11-7082 arrested VSMC proliferation and 10 μM BAY 11-7082 was toxic. On the other hand, HUVEC viability was not affected by BAY11-7082 upto 10 μM. In addition, BAY11-7082 inhibited the activation of NF-κB and expression of IL-6, IL-8, and VCAM-1 without toxic effect. Conclusions: NF-κB inhibition using BAY11-7082 can contribute the protection of neointima formation by blocking proliferation of VSMC, while potentiate endothelial cells from TNF-α stimulation.
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