Porphyromonas gingivalis-Induced MIF Regulates Intercellular Adhesion Molecule-1 Expression in EA.hy926 Cells and Monocyte-Endothelial Cell Adhesion Through the Receptors CD74 and CXCR4
Yun WuWanyue XuJingya HouYanqing LiuRong LiJingbo LiuChen LiXiaolin TangLi LinYaping PanDongmei Zhang
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Abstract:
Porphyromonas gingivalis (P. gingivalis) is an important pathogen that contributes to periodontal disease and causes infections that promote the progression of atherosclerosis. Our previous studies showed that macrophage migration inhibitory factor (MIF) facilitates monocyte adhesion to endothelial cells by regulating the expression of intercellular adhesion molecule-1 (ICAM-1) in P. gingivalis-infected endothelial cells. However, the detailed pathological role of MIF has yet to be elucidated in this context. To explore the functional receptor(s) of MIF that underlie its participation in the pathogenesis of atherosclerosis, we investigated the expression of the chemokine receptors CD74 and CXCR4 in endothelial cells, both of which were shown to be involved in the adhesion of monocytes to endothelial cells pretreated with P. gingivalis. Furthermore, the formation of a MIF, CD74, and CXCR4 ligand-receptor complex was revealed by our immunofluorescence staining and coimmunoprecipitation results. By interacting with the CD74/CXCR4 receptor complex, MIF may act as a crucial regulator of monocyte-endothelial cell adhesion and promote the atherosclerotic plaque formation induced by P. gingivalis.Keywords:
Monocyte
Intercellular adhesion molecule
Aim To explore the mechanisms of influenza virus infection in the formation of atherosclerosis from the cellular and molecular levels through investigating amount of intercellular adhesion molecule-1and vascular cell adhesion molecule-1after human umbilical vein endothelial cell was infected by influenza virus. Methods SYBR Green reverse transcription polymerase chain reaction(RT-PCR),flow cytometry and enzyme-linked immunosorbent assay were used to detect the timing expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 of human umbilical vein endothelial cells infected by influenza virus at 0 h,24 h,48 h and 72 h. Results Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1were measured by these three methods after human umbilical vein endothelial cell was infected by influenza virus.The base level of the two inflammatory factors was expressed at a low level at 0 h,and began to increase after influenza virus infection,reached the peak at 24 h.After 48 h,it declined obviously and remained a relatively high level at 72 h.The amount of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in the infected groups was higher than that in the control group(P﹤0.05). Conclusion This study showed that influenza virus infection could increase the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1,and then influenza virus infection might lead to dysfunction of vascular endothelial cells and involve in the inflammatory response of atherosclerosis.
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Abstract Endothelial cells (EC) recruit circulating leukocytes to sites of inflammation, partly by expression of endothelial-leukocyte adhesion molecules. Whereas the regulation of some adhesion molecules is well characterized in cultured HUVEC, similar data for microvascular human test systems are limited. We studied the cytokine-regulated expression of vascular cell adhesion molecules E-selectin, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in cultured human intestinal microvascular endothelial cells (HIMEC). E-selectin and VCAM-1 were induced, and ICAM-1 was enhanced, in a dose-dependent fashion after stimulation with IL-1beta, TNF-alpha, and LPS. Each adhesion molecule displayed characteristic time-related responses comparable to those obtained with HUVEC, and each molecule supported adhesion of leukocytes. Notable disparities between the two endothelial test systems were that 1) expression of total cellular E-selectin (but not surface membrane expression) was sustained after 72 h of IL-1beta stimulation in HIMEC, contrasting a rapid biphasic response in HUVEC; 2) LPS did not maintain prolonged expression of ICAM-1 and VCAM-1 in HIMEC; and 3) VCAM-1 protein was dose-dependently up-regulated by IL-4 in HUVEC, peaking after 8 h, while IL-4 had only a negligible effect on the expression of this protein in HIMEC. In conclusion, the regulation of these adhesion molecules appears to be somewhat different in HIMEC compared with HUVEC, and the differences from available data on skin-derived microvascular endothelial cell cultures are to some extent substantial. Our findings document the importance of using relevant endothelial cell culture systems for studies of leukocyte-endothelial cell interactions.
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To determine whether 17 beta-estradiol, progesterone, and prostaglandin (PG) E2, alone or in combination with cytokines, influence the adhesiveness of vascular endothelium and thus play a role in the first stage of leukocyte infiltration of the uterine cervix during parturition.Cultured umbilical vein endothelial cells obtained from 11 women after vaginal delivery at term were incubated with 17 beta-estradiol, progesterone, PGE2, tumor necrosis factor alpha (TNF-alpha), and interleukin-8, (IL-8), alone and in combination. The expression of endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 was investigated by immunofluorescence and flow cytometry. The Kolmogorov-Smirnov test was used for statistical analysis.We found that 17 beta-estradiol augmented the TNF-alpha-induced expression of endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 by 107, 9, and 39%, respectively. Alone, 17 beta-estradiol induced the expression of only intercellular adhesion molecule-1 (24%), as did PGE2 (13%). Neither progesterone nor IL-8 induced expression of any of these adhesion molecules.Unlike progesterone, 17 beta-estradiol and PGE2 stimulate the expression of adhesion molecules in vitro and may, therefore, promote adhesion of granulocytes to capillary endothelium.
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Carbamylated low-density lipoprotein (LDL), the most abundant modified LDL isoform in human blood, has been recently implicated in causing the atherosclerosis-prone injuries to endothelial cells in vitro and atherosclerosis in humans. This study was aimed at testing the hypothesis that carbamylated LDL acts via inducing monocyte adhesion to endothelial cells and determining the adhesion molecules responsible for the recruitment of monocytes.Exposure of human coronary artery endothelial cells with carbamylated LDL but not native LDL caused U937 monocyte adhesion and the induction of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 adhesion molecules as measured by cell enzyme-linked immunosorbent assay. Silencing of intercellular adhesion molecule-1 by siRNA or its inhibition using neutralizing antibody resulted in decreased monocyte adhesion to the endothelial cells. Similar silencing or neutralizing of vascular cell adhesion molecule-1 alone did not have an effect but was shown to contribute to intercellular adhesion molecule-1 when tested simultaneously.Taken together, these data provide evidence that intercellular adhesion molecule-1 in cooperation with vascular cell adhesion molecule-1 are essential for monocyte adhesion by carbamylated low-density lipoprotein-activated human vascular endothelial cells in vitro.
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