Gene expression profiles of glucose toxicity-exposed islet microvascular endothelial cells

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 7 ◽  
pp. 157-165 ◽  
Author(s):  
Zhengda Sun ◽  
Devon A. Lawson ◽  
Elizabeth Sinclair ◽  
Chih-Yang Wang ◽  
Ming-Derg Lai ◽  
...  

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 240 ◽  
Author(s):  
Abha Sahni ◽  
Hema Narra ◽  
Jignesh Patel ◽  
Sanjeev Sahni

Microvascular endothelial cells (ECs) represent the primary target cells during human rickettsioses and respond to infection via the activation of immediate–early signaling cascades and the resultant induction of gene expression. As small noncoding RNAs dispersed throughout the genome, microRNAs (miRNAs) regulate gene expression post-transcriptionally to govern a wide range of biological processes. Based on our recent findings demonstrating the involvement of fibroblast growth factor receptor 1 (FGFR1) in facilitating rickettsial invasion into host cells and published reports suggesting miR-424 and miR-503 as regulators of FGF2/FGFR1, we measured the expression of miR-424 and miR-503 during R. conorii infection of human dermal microvascular endothelial cells (HMECs). Our results revealed a significant decrease in miR-424 and miR-503 expression in apparent correlation with increased expression of FGF2 and FGFR1. Considering the established phenomenon of endothelial heterogeneity and pulmonary and cerebral edema as the prominent pathogenic features of rickettsial infections, and significant pathogen burden in the lungs and brain in established mouse models of disease, we next quantified miR-424 and miR-503 expression in pulmonary and cerebral microvascular ECs. Again, R. conorii infection dramatically downregulated both miRNAs in these tissue-specific ECs as early as 30 min post-infection in correlation with higher FGF2/FGFR1 expression. Changes in the expression of both miRNAs and FGF2/FGFR1 were next confirmed in a mouse model of R. conorii infection. Furthermore, miR-424 overexpression via transfection of a mimic into host ECs reduced the expression of FGF2/FGFR1 and gave a corresponding decrease in R. conorii invasion, while an inhibitor of miR-424 had the expected opposite effect. Together, these findings implicate the rickettsial manipulation of host gene expression via regulatory miRNAs to ensure efficient cellular entry as the critical requirement to establish intracellular infection.


2009 ◽  
Vol 136 (5) ◽  
pp. A-698-A-699
Author(s):  
Amrita Ahluwalia ◽  
Xiaoming Deng ◽  
Vipal Gandhi ◽  
Sushrut S. Thiruvengadam ◽  
Andrzej S. Tarnawski

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