Fibronectin and vitronectin induce AP-1-mediated matrix metalloproteinase-9 expression through integrin α5β1/αvβ3-dependent Akt, ERK and JNK signaling pathways in human umbilical vein endothelial cells

2011 ◽  
Vol 23 (1) ◽  
pp. 125-134 ◽  
Author(s):  
Young-June Jin ◽  
Iha Park ◽  
In-Kee Hong ◽  
Hee-Jung Byun ◽  
Jeongsuk Choi ◽  
...  
Vascular ◽  
2021 ◽  
pp. 170853812198985
Author(s):  
Chen Wang ◽  
Yanqin Zhang ◽  
Zhenxing Jiang ◽  
Huiling Bai ◽  
Zizhong Du

Objective Thromboangiitis obliterans is a nonatherosclerotic segmental inflammatory disease, and miR-100 plays an anti-inflammatory role in chronic inflammation. Therefore, we hypothesized that miR-100 might alleviate the inflammatory damage and apoptosis of H2O2-induced ECV304 cells and aimed to investigate the relationship between miR-100 and thromboangiitis obliterans and the related molecular mechanism. Methods Cell counting kit-8 was used to detect cell viability, and the expression of inflammatory factors and oxidative stress was measured by ELISA. TUNEL assay was used to detect the apoptosis of human umbilical vein endothelial cells after induction by H2O2. Furthermore, the interaction between miR-100 and matrix metalloproteinase-9 was verified by dual-luciferase assay. Quantitative reverse transcription polymerase chain reaction and western blot were used to detect the expression of the adhesion factors, apoptosis-related proteins and Notch pathway-related protein. Results The results revealed that miR-100 was decreased in H2O2-induced human umbilical vein endothelial cells. Overexpression of miR-100 attenuated inflammatory response and cell apoptosis in H2O2-induced human umbilical vein endothelial cells. The overexpression of miR-100 inhibited matrix metalloproteinase-9 expression in H2O2-induced human umbilical vein endothelial cells. miR-100 inhibited H2O2-induced human umbilical vein endothelial cell inflammation, oxidative stress, and cell apoptosis via inactivation of Notch signaling by targeting matrix metalloproteinase. Conclusions Our study demonstrated that miR-100 reduced the inflammatory damage and apoptosis of H2O2-induced human umbilical vein endothelial cells via inactivation of Notch signaling by targeting matrix metalloproteinase. These findings suggested that miR-100 might be a novel therapeutic target for the prevention of thromboangiitis obliterans.


2019 ◽  
Vol 60 (1) ◽  
pp. 62-69
Author(s):  
Wei Jiang ◽  
Ping Liu ◽  
Jianlei Zhang ◽  
Wenjie Yang

AbstractCandida albicans is a common opportunistic pathogen that can cause serious infection by blood transmission. C. albicans enters the blood circulation and adheres to the endothelial cells of the vascular wall. However, the detailed mechanism of the effect of C. albicans on the endothelial cells remains unclear. In this study, the microarray expression profile of human umbilical vein endothelial cells exposed to C. albicans was analyzed. The 191 up-regulated genes were enriched in TNF, T cell receptor, and NF-kappa B signaling pathways. The 71 down-regulated genes were enriched in pyruvate metabolic, purine nucleotide metabolic, purine nucleotide biosynthetic, and humoral immune response processes. Gene set enrichment analysis showed that apoptosis, oxidative phosphorylation, IL6/JAK/STAT3 signaling pathways were enriched. Moreover, two hub genes with a high degree of connectivity, namely, MYC and IL6, were selected. Molecular screening of traditional Chinese medicine libraries was performed on the basis of the structure of MYC protein. The okanin had the highest docking score. MYC might be used as molecular targets for treatment. In addition, okanin may inhibit the infection of C. albicans. Thus, MYC can be subjected to further research.


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