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English Abstract
Journal Article
Research Support, Non-U.S. Gov't
[The effect of TLR4/NF-kappaB activation and LOX-1 on monocyte adhesion to endothelium].
Zhonghua Xin Xue Guan Bing za Zhi 2005 September
OBJECTIVE: Recent studies have shown that Toll-like receptor 4 (TLR4), a mediator of for innate immune responses, is involved in the initiation and progression of atherosclerosis. TLR4 activation mediates the expression of chemokines and cytokines through activation of NF-kappaB. We investigated the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), intercellular adhesion molecule-1 (CAM-1), E-selectin induced by TLR4/NF-kappaB in human umbilical vein endothelial cells (HUVECs), and their effects on adhesion of monocyte to HUVECs.
METHODS: HUVECs were incubated with purified LPS for 24 h. TLR4, LOX-1, ICAM-1, E-selectin mRNA were measured by RT-PCR; the protein expression of TLR4, LOX-1 and activation of NF-kappaB were detected by Western blot; the adhesive percentage between HUVECs and monocytes was determined by direct counting.
RESULTS: LPS (1 mg/L) not only enhanced expression of TLR4, activation of NF-kappaB and induction of LOX-1, ICAM-1, E-selectin expression, but also increased the percentage of monocyte adhesion to endothelium. Pretreatment of HUVECs with anti-LOX1, anti-ICAM-1 or anti E-selectin antibodies partly abolished the increase in monocyte adhesion to endothelium. NF-kappaB inhibitor CAPE suppressed LPS-induced these effects.
CONCLUSION: TLR4/NF-kappaB plays an important role in monocyte-endothelium adhesion partly through upregulation of LOX-1, ICAM-1 and E-selection expression, which may provide a target for the treatment of atherosclerosis.
METHODS: HUVECs were incubated with purified LPS for 24 h. TLR4, LOX-1, ICAM-1, E-selectin mRNA were measured by RT-PCR; the protein expression of TLR4, LOX-1 and activation of NF-kappaB were detected by Western blot; the adhesive percentage between HUVECs and monocytes was determined by direct counting.
RESULTS: LPS (1 mg/L) not only enhanced expression of TLR4, activation of NF-kappaB and induction of LOX-1, ICAM-1, E-selectin expression, but also increased the percentage of monocyte adhesion to endothelium. Pretreatment of HUVECs with anti-LOX1, anti-ICAM-1 or anti E-selectin antibodies partly abolished the increase in monocyte adhesion to endothelium. NF-kappaB inhibitor CAPE suppressed LPS-induced these effects.
CONCLUSION: TLR4/NF-kappaB plays an important role in monocyte-endothelium adhesion partly through upregulation of LOX-1, ICAM-1 and E-selection expression, which may provide a target for the treatment of atherosclerosis.
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