scholarly journals G protein-coupled estrogen receptor-mediated effects on cytosolic calcium and nanomechanics in brain microvascular endothelial cells

2015 ◽  
Vol 133 (5) ◽  
pp. 629-639 ◽  
Author(s):  
Joseph B. Altmann ◽  
Guang Yan ◽  
Jeffrey F. Meeks ◽  
Mary E. Abood ◽  
Eugen Brailoiu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Estrogen Receptor ◽  
G Protein ◽  
Cytosolic Calcium ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Mediated Effects ◽  
Microvascular Endothelial ◽  
G Protein Coupled

scholarly journals GPR55-mediated effects on brain microvascular endothelial cells and the blood–brain barrier

Neuroscience ◽  
2019 ◽  
Vol 414 ◽  
pp. 88-98 ◽  
Author(s):  
Luciana M. Leo ◽  
Boluwatife Familusi ◽  
Michelle Hoang ◽  
Raymond Smith ◽  
Kristen Lindenau ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Mediated Effects ◽  
Blood Brain ◽  
Microvascular Endothelial

Inflammatory stress increases receptor for lysophosphatidylcholine in human microvascular endothelial cells

2003 ◽  
Vol 285 (4) ◽  
pp. H1786-H1789 ◽  
Author(s):  
Hazel Lum ◽  
Jing Qiao ◽  
Robert J. Walter ◽  
Fei Huang ◽  
Papasani V. Subbaiah ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
G Protein ◽  
Cell Monolayer ◽  
Microvascular Endothelial Cells ◽  
Pcr Analysis ◽  
Binding Studies ◽  
Tnf Α ◽  
Microvascular Endothelial ◽  
G Protein Coupled

The atherogenic serum lysophosphatidylcholine (LPC) is known to mediate vascular endothelial responses ranging from upregulation of adhesion molecules and growth factors to secretion of chemokines and superoxide anion. We investigated whether endothelial cells express receptors for LPC, which may account for their actions. Human brain microvascular (HBMEC) and dermal microvascular endothelial cells (HMEC) were prepared for RT-PCR analysis for possible expression of the G protein-coupled receptors, GPR4 and G2A, which are believed to be specific LPC receptors. Results indicated that HBMEC expressed low basal GPR4 mRNA, but stimulation with tumor necrosis factor-α (TNF-α) (100 U/ml) or H2O2 (50 μmol/l) for 2 h or overnight upregulated expression severalfold. In contrast, HMEC expressed high basal GPR4 mRNA, which was not further increased by either TNF-α or H2O2 stimulation. Another LPC receptor, G2A, was not detected in either endothelial cell type. Competition binding studies were made to evaluate specific binding of [3H]LPC to the intact endothelial cell monolayer. Basal specific [3H]LPC binding in HBMEC was approximately eight times lower than in HMEC; however, TNF-α or H2O2 stimulation increased [3H]LPC binding on HMBEC but not HMEC. The results indicated that GPR4 expression was consistent with specific [3H]LPC binding. Overall, we report that endothelial cells selectively expressed GPR4, a specific LPC receptor. Furthermore, GPR4 expression by HBMEC, but not HMEC, was increased by inflammatory stresses. We conclude that endogenous GPR4 in endothelial cells may be a potential G protein-coupled receptor by which LPC signals proinflammatory activities.

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.

Sign in / Sign up

Export Citation Format

Share Document