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Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro
Published on: November 26, 2018
MicroRNA-155 contributes to shear-resistant leukocyte adhesion to human brain endothelium in vitro
Camilla Cerutti1,2, Patricia Soblechero-Martin3, Dongsheng Wu3,4
1Department of Life, Health and Chemical Sciences, Biomedical Research Network, Open University, Walton Hall, Milton Keynes, MK7 6AA, UK. Camilla.cerutti@kcl.ac.uk.
Background:
Increased leukocyte adhesion to brain endothelial cells forming the blood-brain barrier (BBB) precedes extravasation into the central nervous system (CNS) in neuroinflammatory diseases such as multiple sclerosis (MS). Previously, we reported that microRNA-155 (miR-155) is up-regulated in MS and by inflammatory cytokines in human brain endothelium, with consequent modulation of endothelial paracellular permeability. Here, we investigated the role of endothelial miR-155 in leukocyte adhesion to the human cerebral microvascular endothelial cell line, hCMEC/D3, under shear forces mimicking blood flow in vivo.
Results:
Using a gain- and loss-of-function approach, we show that miR-155 up-regulation increases leukocyte firm adhesion of both monocyte and T cells to hCMEC/D3 cells. Inhibition of endogenous endothelial miR-155 reduced monocytic and T cell firm adhesion to naïve and cytokines-induced human brain endothelium. Furthermore, this effect is partially associated with modulation of the endothelial cell adhesion molecules VCAM1 and ICAM1 by miR-155.
Conclusions:
Our results suggest that endothelial miR-155 contribute to the regulation of leukocyte adhesion at the inflamed BBB. Taken together with previous observations, brain endothelial miR-155 may constitute a potential molecular target for treatment of neuroinflammation diseases.
Insights
MicroRNA-155 (miR-155) in brain endothelial cells promotes leukocyte adhesion to the blood-brain barrier (BBB). Inhibiting miR-155 reduces this adhesion, suggesting it’s a target for neuroinflammation treatment.
Area of Science:
- Neuroimmunology
- Endothelial Biology
- Molecular Medicine
Background:
- Leukocyte adhesion to brain endothelial cells at the blood-brain barrier (BBB) is critical in neuroinflammation, as seen in multiple sclerosis (MS).
- MicroRNA-155 (miR-155) is upregulated in MS and by inflammatory cytokines in brain endothelium, affecting BBB permeability.
- Previous work indicated miR-155's role in endothelial permeability; this study focuses on its impact on leukocyte adhesion.
Purpose of the Study:
- To investigate the role of endothelial miR-155 in leukocyte adhesion to human brain endothelium under physiological shear forces.
- To determine if miR-155 influences the adhesion of monocytes and T cells to the BBB.
Main Methods:
- Utilized a gain- and loss-of-function approach in the hCMEC/D3 human brain endothelial cell line.
- Applied shear forces mimicking in vivo blood flow to study leukocyte adhesion.
- Assessed the expression of cell adhesion molecules VCAM1 and ICAM1.
Main Results:
- Upregulation of miR-155 significantly increased firm adhesion of monocytes and T cells to endothelial cells.
- Inhibition of endogenous miR-155 reduced leukocyte firm adhesion under both basal and cytokine-induced conditions.
- The observed effects were partially linked to miR-155's modulation of VCAM1 and ICAM1 expression.
Conclusions:
- Endothelial miR-155 plays a regulatory role in leukocyte adhesion at the inflamed BBB.
- Brain endothelial miR-155 represents a potential therapeutic target for treating neuroinflammatory diseases.
- These findings complement previous research on miR-155's involvement in BBB dysfunction.
