scholarly journals Sera from patients with falciparum malaria induce substance P gene expression in cultured human brain microvascular endothelial cells.

1996 ◽  
Vol 64 (12) ◽  
pp. 5106-5110 ◽  
Author(s):  
C B Chiwakata ◽  
G Hort ◽  
C J Hemmer ◽  
M Dietrich
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Substance P ◽  
Human Brain ◽  
Falciparum Malaria ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
P Gene ◽  
Microvascular Endothelial

scholarly journals Infectomic Analysis of Gene Expression Profiles of Human Brain Microvascular Endothelial Cells Infected withCryptococcus neoformans

2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
Ambrose Jong ◽  
Chun-Hua Wu ◽  
Wensheng Zhou ◽  
Han-Min Chen ◽  
Sheng-He Huang
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Human Brain ◽  
Time Course ◽  
Expression Profiles ◽  
Host Cells ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Microvascular Endothelial ◽  
Time Point

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.

scholarly journals Transcriptome analysis of human brain microvascular endothelial cells response to Neisseria meningitidis and its antigen MafA using RNA-seq

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Evelína Káňová ◽  
Zuzana Tkáčová ◽  
Katarína Bhide ◽  
Amod Kulkarni ◽  
Irene Jiménez-Munguía ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Human Brain ◽  
Neisseria Meningitidis ◽  
Global Gene Expression ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Biological Processes ◽  
Rna Seq ◽  
Microvascular Endothelial

AbstractInteraction of Neisseria meningitidis (NM) with human brain microvascular endothelial cells (hBMECs) initiates of multiple cellular processes, which allow bacterial translocation across the blood-brain barrier (BBB). NM is equipped with several antigens, which interacts with the host cell receptors. Recently we have shown that adhesin MafA (UniProtKB-X5EG71), relatively less studied protein, is one of those surface exposed antigens that adhere to hBMECs. The present study was designed to comprehensively map the undergoing biological processes in hBMECs challenged with NM or MafA using RNA sequencing. 708 and 726 differentially expressed genes (DEGs) were identified in hBMECs exposed to NM and MafA, respectively. Gene ontology analysis of the DEGs revealed that several biological processes, which may alter the permeability of BBB, were activated. Comparative analysis of DEGs revealed that MafA, alike NM, might provoke TLR-dependent pathway and augment cytokine response. Moreover, both MafA and NM were able to induce genes involved in cell surface modifications, endocytosis, extracellular matrix remodulation and anoikis/apoptosis. In conclusion, this study for the first time describes effect of NM on the global gene expression in hBMECs using high-throughput RNA-seq. It also presents ability of MafA to induce gene expression, which might aid NM in breaching the BBB.

scholarly journals Altered Gene Expression in Human Brain Microvascular Endothelial Cells in Response to the Infection of Influenza H1N1 Virus

2021 ◽  
Author(s):  
Doaa Higazy ◽  
Xianwu Lin ◽  
Tanghui Xie ◽  
Ke Wang ◽  
Xiaochen Gao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Human Brain ◽  
Influenza A Virus ◽  
Influenza A ◽  
H1n1 Virus ◽  
Influenza Viruses ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Microvascular Endothelial

Abstract Influenza viruses are not only causing respiratory illness, but also neurological manifestations were reported following acute viral infection. The Central nervous system (CNS) has a specific defence mechanism against pathogens structured by cerebral microvasculature lined with brain endothelial cells to form the blood-brain barrier (BBB). To investigate the response of human brain microvascular endothelial cells (hBMECs) to the influenza A virus, we inoculated the cells with the A/WSN/33 (H1N1) virus. We then conducted an RNAseq experiment to determine the changes in gene expression levels and the activated disease pathways following infection. The analysis revealed an effective activation of the innate immune defence by inducing the pattern recognition receptors (PRRs). Along with the production of proinflammatory cytokines, we detected an upregulation of interferons and interferon-stimulated genes, such as IFN-β/λ, ISG15, CXCL11, CXCL3, and IL-6, etc. Moreover, infected hBMECs exhibited a disruption in the cytoskeletal structure both on the transcriptomic and cellular levels. We also noted that pathways of neuroactive ligand-receptor interaction, neuroinflammation, and neurodegenerative diseases were noticeably induced together with a predicted activation of the neuroglia. Likewise, a number of genes linked with the mitochondrial structure and function display a significant differential expression. En masse, this data supports that hBMECs could be infected by the influenza A virus, which induces the innate and inflammatory immune response. The results suggest that the influenza virus infection could potentially induce a subsequent aggravation of neurological disorders.

scholarly journals Ubiquinone Metabolism and Transcription HIF-1 Targets Pathway Are Toxicity Signature Pathways Present in Extracellular Vesicles of Paraquat-Exposed Human Brain Microvascular Endothelial Cells

2021 ◽  
Vol 22 (10) ◽  
pp. 5065
Author(s):  
Tatjana Vujić ◽  
Domitille Schvartz ◽  
Anton Iliuk ◽  
Jean-Charles Sanchez
Keyword(s):  
Endothelial Cells ◽  
Human Brain ◽  
Extracellular Vesicles ◽  
Physiological State ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Cell Of Origin ◽  
Functional Changes ◽  
Data Independent Acquisition ◽  
Microvascular Endothelial

Over the last decade, the knowledge in extracellular vesicles (EVs) biogenesis and modulation has increasingly grown. As their content reflects the physiological state of their donor cells, these “intercellular messengers” progressively became a potential source of biomarker reflecting the host cell state. However, little is known about EVs released from the human brain microvascular endothelial cells (HBMECs). The current study aimed to isolate and characterize EVs from HBMECs and to analyze their EVs proteome modulation after paraquat (PQ) stimulation, a widely used herbicide known for its neurotoxic effect. Size distribution, concentration and presence of well-known EV markers were assessed. Identification and quantification of PQ-exposed EV proteins was conducted by data-independent acquisition mass spectrometry (DIA-MS). Signature pathways of PQ-treated EVs were analyzed by gene ontology terms and pathway enrichment. Results highlighted that EVs exposed to PQ have modulated pathways, namely the ubiquinone metabolism and the transcription HIF-1 targets. These pathways may be potential molecular signatures of the PQ-induced toxicity carried by EVs that are reflecting their cell of origin by transporting with them irreversible functional changes.

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