Altered VEGF-A and receptor mRNA expression profiles, and identification of VEGF144 in foetal rat calvaria cells, in coculture with microvascular endothelial cells

2013 ◽  
Vol 37 (7) ◽  
pp. 713-724 ◽  
Author(s):  
Birgit Weyand ◽  
Herbert P. von Schroeder
2018 ◽  
Vol 25 (4) ◽  
pp. e12450 ◽  
Author(s):  
Mingming Liu ◽  
Wenbao Lu ◽  
Qunxing Hou ◽  
Bing Wang ◽  
Youming Sheng ◽  
...  

2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
Ambrose Jong ◽  
Chun-Hua Wu ◽  
Wensheng Zhou ◽  
Han-Min Chen ◽  
Sheng-He Huang

In order to dissect the pathogenesis ofCryptococcus neoformansmeningoencephalitis, a genomic survey of the changes in gene expression of human brain microvascular endothelial cells infected byC.neoformanswas carried out in a time-course study. Principal component analysis (PCA) revealed sigificant fluctuations in the expression levels of different groups of genes during the pathogen-host interaction. Self-organizing map (SOM) analysis revealed that most genes were up- or downregulated 2 folds or more at least at one time point during the pathogen-host engagement. The microarray data were validated by Western blot analysis of a group of genes, includingβ-actin, Bcl-x, CD47, Bax, Bad, and Bcl-2. Hierarchical cluster profile showed that 61 out of 66 listed interferon genes were changed at least at one time point. Similarly, the active responses in expression of MHC genes were detected at all stages of the interaction. Taken together, our infectomic approaches suggest that the host cells significantly change the gene profiles and also actively participate in immunoregulations of the central nervous system (CNS) duringC.neoformansinfection.


2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Meina Shi ◽  
Yingting Liu ◽  
Lixing Feng ◽  
Yingbo Cui ◽  
Yajuan Chen ◽  
...  

Scutellarin (SCU) is one of the main components of traditional Chinese medicine plantErigeron breviscapus (Vant.)Hand.-Mazz. In this paper, we studied the protective effects of SCU on human cardiac microvascular endothelial cells (HCMECs) against hypoxia-reoxygenation (HR) injury and its possible target-related proteins. Results of MTT assay showed that pretreatment of SCU at doses of 1, 5, and 10 μM for 2 h could significantly inhibit the decrease in cell viability of HCMECs induced by HR injury. Subcellular fractions of cells treated with vehicle control, 1 μM SCU, HR injury, or 1 μM SCU + HR injury were separated by ultracentrifugation. The protein expression profiles of cytoplasm and membrane/nuclei fractions were checked using protein two-dimensional electrophoresis (2-DE). Proteins differentially expressed between control and SCU-treated group, control and HR group, or HR and SCU + HR group were identified using mass spectrometry (MS/MS). Possible interaction network of these target-related proteins was predicted using bioinformatic analysis. The influence of SCU on the expression levels of these proteins was confirmed using Western blotting assay. The results indicated that proteins such as p27BBP protein (EIF6), heat shock 60 kDa protein 1 (HSPD1), and chaperonin containing TCP1 subunit 6A isoform (CCT6A) might play important roles in the effects of SCU.


1991 ◽  
Vol 97 (4) ◽  
pp. 618-623 ◽  
Author(s):  
Helen A. Bull ◽  
Christopher B. Bunker ◽  
Georgio. Terenghi ◽  
David R. Springall ◽  
Yidan. Zhao ◽  
...  

2021 ◽  
Vol 27 ◽  
Author(s):  
Rui Zhang ◽  
Xiaoying Ma ◽  
Lei Jiang ◽  
Wenzhen Xia ◽  
Haipeng Li ◽  
...  

Background: This study was performed to identify the alterations of Long non-coding RNAs (lncRNAs) induced by oxidative stress and investigate the functional roles of SNHG16 in the pathological angiogenesis by human retinal microvascular endothelial cells (HMRECs). Methods: The expression profiles of lncRNAs and mRNAs induced by oxidative stress were identified by RNA-Seq, and the dysregulation of 16 lncRNAs including SNHG16 were verified in H2O2-treated human umbilical vein endothelial cells (HUVECs). Luciferase reporter assay and RIP analysis were used to investigate the binding relationship of SNHG16 to miR-195. Results: We confirmed that over-expression of SNGH16 attenuated H2O2-induced angiogenesis by HMRECs. In addition, SNHG16 was significantly decreased whereas miR-195, a predictive target of SNHG16, was upregulated in H2O2, HG, and AGE-treated HMRECs. The binding relationship of SNHG16 to miR-195 was subsequently verified by luciferase reporter assay and RIP analysis. SNHG16 cotransfection abolished miR-195-mediated repression on mitofusin 2 (mfn2) protein level and counteracted the inductive effect of miR-195 on angiogenesis by HMRECs. Conclusion: These results indicated that decreased SNHG16 accelerates oxidative stress induced pathological angiogenesis in HMRECs by regulating miR-195/mfn2 axis, providing a potential target for diabetic retinopathy (DR) therapy.


2012 ◽  
Vol 82 (4) ◽  
pp. 267-274 ◽  
Author(s):  
Zahide Cavdar ◽  
Mehtap Y. Egrilmez ◽  
Zekiye S. Altun ◽  
Nur Arslan ◽  
Nilgun Yener ◽  
...  

The main pathophysiology in cerebral ischemia is the structural alteration in the neurovascular unit, coinciding with neurovascular matrix degradation. Among the human matrix metalloproteinases (MMPs), MMP-2 and -9, known as gelatinases, are the key enzymes for degrading type IV collagen, which is the major component of the basal membrane that surrounds the cerebral blood vessel. In the present study, we investigated the effects of resveratrol on cytotoxicity, reactive oxygen species (ROS), and gelatinases (MMP-2 and -9) in human cerebral microvascular endothelial cells exposed to 6 hours of oxygen-glucose deprivation and a subsequent 24 hours of reoxygenation with glucose (OGD/R), to mimic ischemia/reperfusion in vivo. Lactate dehydrogenase increased significantly, in comparison to that in the normoxia group. ROS was markedly increased in the OGD/R group, compared to normoxia. Correspondingly, ROS was significantly reduced with 50 μM of resveratrol. The proMMP-2 activity in the OGD/R group showed a statistically significant increase from the control cells. Resveratrol preconditioning decreased significantly the proMMP-2 in the cells exposed to OGD/R in comparison to that in the OGD/R group. Our results indicate that resveratrol regulates MMP-2 activity induced by OGD/R via its antioxidant effect, implying a possible mechanism related to the neuroprotective effect of resveratrol.


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