Faculty Opinions recommendation of Galantamine and carbon monoxide protect brain microvascular endothelial cells by heme oxygenase-1 induction.

2008 ◽  
Author(s):  
George Perry
Keyword(s):  
Carbon Monoxide ◽  
Endothelial Cells ◽  
Heme Oxygenase ◽  
Microvascular Endothelial Cells ◽  
Heme Oxygenase 1 ◽  
Brain Microvascular Endothelial Cells ◽  
Microvascular Endothelial

Galantamine and carbon monoxide protect brain microvascular endothelial cells by heme oxygenase-1 induction

2008 ◽  
Vol 367 (3) ◽  
pp. 674-679 ◽  
Author(s):  
Atsunori Nakao ◽  
David J. Kaczorowski ◽  
Brian S. Zuckerbraun ◽  
Jing Lei ◽  
Gaetano Faleo ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Endothelial Cells ◽  
Heme Oxygenase ◽  
Microvascular Endothelial Cells ◽  
Heme Oxygenase 1 ◽  
Brain Microvascular Endothelial Cells ◽  
Microvascular Endothelial

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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