scholarly journals Transcriptome Profiling Reveals Pro-Inflammatory Cytokines and Matrix Metalloproteinase Activation in Zika Virus Infected Human Umbilical Vein Endothelial Cells

2019 ◽  
Vol 10 ◽  
Author(s):  
Svetlana Khaiboullina ◽  
Timsy Uppal ◽  
Konstatin Kletenkov ◽  
Stephen Charles St. Jeor ◽  
Ekaterina Garanina ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Matrix Metalloproteinase ◽  
Inflammatory Cytokines ◽  
Zika Virus ◽  
Umbilical Vein ◽  
Transcriptome Profiling ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Pro Inflammatory Cytokines

Activation of pro-(matrix metalloproteinase-2) (pro-MMP-2) by thrombin is membrane-type-MMP-dependent in human umbilical vein endothelial cells and generates a distinct 63 kDa active species

2001 ◽  
Vol 357 (1) ◽  
pp. 107-115 ◽  
Author(s):  
Marc A. LAFLEUR ◽  
Morley D. HOLLENBERG ◽  
Susan J. ATKINSON ◽  
Vera KNÄUPER ◽  
Gillian MURPHY ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Matrix Metalloproteinase ◽  
Umbilical Vein ◽  
Coagulation Cascade ◽  
Matrix Metalloproteinase 2 ◽  
Intermediate Form ◽  
Dependent Manner ◽  
Human Umbilical Vein ◽  
Membrane Type ◽  
Umbilical Vein Endothelial Cells

Thrombin, a critical enzyme in the coagulation cascade, has also been associated with angiogenesis and activation of the zymogen form of matrix metalloproteinase-2 (MMP-2 or gelatinase-A). We show that thrombin activated pro-MMP-2 in a dose- and time-dependent manner in cultured human umbilical-vein endothelial cells (HUVECs) to generate a catalytically active 63kDa protein that accumulated as the predominant form in the conditioned medium. This 63kDa thrombin-activated MMP-2 is distinct from the 62kDa species found following concanavalin A or PMA stimulated pro-MMP-2 activation. Hirudin and leupeptin blocked thrombin-induced pro-MMP-2 activation, demonstrating that the proteolytic activity of thrombin is essential. However, activation was also dependent upon membrane-type-MMP (MT-MMP) action, since it was blocked by EDTA, o-phenanthroline, hydroxamate metalloproteinase inhibitors, tissue inhibitor of metalloproteinase-2 (TIMP-2) and TIMP-4, but not TIMP-1. Thrombin inefficiently cleaved recombinant 72kDa pro-MMP-2, but efficiently cleaved the 64kDa MT-MMP-processed intermediate form in the presence of cells. Thrombin also rapidly (within 1h) increased cellular MT-MMP activity, and at longer time points (>6h) it increased expression of MT1-MMP mRNA and protein. Thus signalling via proteinase-activated receptors (PARs) may play a role in thrombin-induced MMP-2 activation, though this does not appear to involve PAR1, PAR2, or PAR4 in HUVECs. These results indicate that in HUVECs the activation of pro-MMP-2 by thrombin involves increased MT-MMP activity and preferential cleavage of the MT-MMP-processed 64kDa MMP-2 form in the presence of cells. The integration of these proteinase systems in the vascular endothelium may be important during thrombogenesis and tissue remodelling associated with neovascularization.

miR-100 alleviates the inflammatory damage and apoptosis of H2O2-induced human umbilical vein endothelial cells via inactivation of Notch signaling by targeting MMP9

Vascular ◽  
2021 ◽  
pp. 170853812198985
Author(s):  
Chen Wang ◽  
Yanqin Zhang ◽  
Zhenxing Jiang ◽  
Huiling Bai ◽  
Zizhong Du
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Matrix Metalloproteinase ◽  
Notch Signaling ◽  
Umbilical Vein ◽  
Thromboangiitis Obliterans ◽  
Human Umbilical Vein ◽  
Inflammatory Damage ◽  
Umbilical Vein Endothelial Cells ◽  
Metalloproteinase 9

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.

scholarly journals Zika Virus Induces Autophagy in Human Umbilical Vein Endothelial Cells

Viruses ◽  
2018 ◽  
Vol 10 (5) ◽  
pp. 259 ◽  
Author(s):  
Haoran Peng ◽  
Bin Liu ◽  
Toure Yves ◽  
Yanhua He ◽  
Shijie Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Zika Virus ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells
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