Selective human endothelial cell activation by chemokines as a guide to cell homing

Silva, Claire Crola Da; Lamerant-Fayel, Nathalie; Paprocka, Maria; Mitterrand, Michèle; Gosset, David; Duś, Danuta; Kiéda, Claudine

doi:10.1111/j.1365-2567.2008.02906.x

Cited by 36 publications

(26 citation statements)

References 37 publications

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“…In the presence of chemokine gradients, the α-chemokine, CXCL12, exhibits a polarized distribution in favor of the basolateral surface in resting HBMEC followed by redistribution to the apical surface upon cytokine stimulation, resulting in equal binding along the basal and apical surfaces [17]. In this respect it is interesting that the binding of chemokines to endothelial cells derived from different organs can vary greatly [28]. The differential binding of various chemokines to resting and cytokine-activated HBMEC may well reflect changes in the surface charge of endothelial cells and the chemical structure and distribution of glycosaminoglycans in the course of the inflammatory response [29].…”

Section: Resultsmentioning

confidence: 99%

Differential Regulation of CD4+ T Cell Adhesion to Cerebral Microvascular Endothelium by the β-Chemokines CCL2 and CCL3

Liu

Dorovini-Zis

2012

IJMS

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In Multiple sclerosis (MS), circulating lymphocytes cross the blood–brain barrier (BBB) and accumulate at sites of antigenic challenge. This process depends on specific interactions between lymphocytes and cerebral microvascular endothelium that involve endothelial activation by cytokines and the presence of chemokines. Chemokines play a key role in the orchestration of immune responses, acting both as chemoattractants and activators of leukocyte subsets. In the present study, we investigated the effects of the β-chemokines, CCL2 and CCL3, on the adhesion of CD4+ T cell subsets to human brain microvessel endothelial cells (HBMEC). Chemokines added to the lower compartment of a two-chamber chemotaxis system under confluent resting or cytokine-activated HBMEC, diffused through the culture substrate and bound to the basal surface of HBMEC. The low rate of adhesion of naïve, resting and memory CD4+ T cells to resting HBMEC was significantly upregulated following treatment of HBMEC with TNF-α and IFN-γ. Recently activated CD4+ T cells readily adhered to resting monolayers. Concentration gradients of CCL2 upregulated the adhesion of activated CD4+ T cells to cytokine treated but not resting HBMEC. The presence of CCL3 in the lower chamber increased the adhesion of memory T cells to both unstimulated and cytokine-treated HBMEC. These findings emphasize the importance of brain endothelial cell activation and the role of CCL2 and CCL3 in regulating the adhesion of CD4+ T cell subsets to BBB endothelium, thus contributing to the specificity of immune responses in MS.

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Section: Resultsmentioning

confidence: 99%

Differential Regulation of CD4+ T Cell Adhesion to Cerebral Microvascular Endothelium by the β-Chemokines CCL2 and CCL3

Liu

Dorovini-Zis

2012

IJMS

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“…Both cancer cells and normal cells were used. The HSkMEC (Human Skin Microvascular Endothelial Cells) cell line was obtained from Cell Culture Collection of the IIET (Wroclaw, Poland) (Crola Da Silva et al 2009). The B16F0 mouse melanoma cancer cell line was obtained from the American Type Culture Collection (ATCC, USA).…”

Section: Characterisationmentioning

confidence: 99%

Structural, spectroscopic and cytotoxicity studies of TbF3@CeF3 and TbF3@CeF3@SiO2 nanocrystals

et al. 2013

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Terbium fluoride nanocrystals, covered by a shell, composed of cerium fluoride were synthesized by a co-precipitation method. Their complex structure was formed spontaneously during the synthesis. The surface of these core/shell nanocrystals was additionally modified by silica. The properties of TbF3@CeF3 and TbF3@CeF3@SiO2 nanocrystals, formed in this way, were investigated. Spectroscopic studies showed that the differences between these two groups of products resulted from the presence of the SiO2 shell. X-ray diffraction patterns confirmed the trigonal crystal structure of TbF3@CeF3 nanocrystals. High resolution transmission electron microscopy in connection with energy-dispersive X-ray spectroscopy showed a complex structure of the formed nanocrystals. Crystallized as small discs, ‘the products’, with an average diameter around 10 nm, showed an increase in the concentration of Tb3+ ions from surface to the core of nanocrystals. In addition to photo-physical analyses, cytotoxicity studies were performed on HSkMEC (Human Skin Microvascular Endothelial Cells) and B16F0 mouse melanoma cancer cells. The cytotoxicity of the nanomaterials was neutral for the investigated cells with no toxic or antiproliferative effect in the cell cultures, either for normal or for cancer cells. This fact makes the obtained nanocrystals good candidates for biological applications and further modifications of the SiO2 shell.Graphical Abstract.

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“…Previous studies have demonstrated that CCL21 is expressed by lymph node endothelial cells and functions as an endothelial cell growth factor (3). Expression of CCL21 is associated with formation of tertiary lymphoid tissue, a process called lymphoid neogenesis (4).…”

mentioning

confidence: 99%

Role of the CCL21 and CCR7 pathways in rheumatoid arthritis angiogenesis

Pickens¹,

Chamberlain²,

Volin³

et al. 2012

Arthritis & Rheumatism

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Objective These studies were performed to determine the role of CCL21 and its corresponding receptor CCR7 in the pathogenesis of Rheumatoid Arthritis (RA). Methods Histological studies were performed to compare the expression of CCR7 and CCL21 in RA synovial tissues. Next the role of CCL21 and/or CCR7 in angiogenesis was examined employing in vitro chemotaxis, tube formation and in vivo matrigel plug assays. Finally the mechanism by which CCL21 mediates angiogenesis was determined by Western blot analysis, endothelial chemotaxis and tube formation. Results In this study, we document that CCR7 and CCL21 colocolize in VWF+ cells where their expression is elevated in RA synovial tissue. Hence the ability to induce angiogenesis was examined for CCR7 ligands, CCL19 and CCL21. CCL21, but not CCL19, at concentrations present in the RA joint, induces human microvascular endothelial cell (HMVEC) migration that is mediated through CCR7 ligation. Further, suppression of the PI3K pathway markedly reduces CCL21-induced HMVEC chemotaxis and tube formation, however suppression of ERK and JNK pathways has no effect on these processes. Neutralization of either CCL21 in RA synovial fluids or CCR7 on HMVECs significantly reduces the induction of HMVEC migration and/or tube formation by RA synovial fluid. We further demonstrate that CCL21 is angiogenic, by showing its ability to promote blood vessel growth in matrigel plugs in vivo at concentrations present in RA joint. Conclusion These observations identify a novel function for CCL21 as an angiogenic mediator in RA, supporting CCL21/CCR7 as a therapeutic target in RA.

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Selective human endothelial cell activation by chemokines as a guide to cell homing

Cited by 36 publications

References 37 publications

Differential Regulation of CD4+ T Cell Adhesion to Cerebral Microvascular Endothelium by the β-Chemokines CCL2 and CCL3

Differential Regulation of CD4+ T Cell Adhesion to Cerebral Microvascular Endothelium by the β-Chemokines CCL2 and CCL3

Structural, spectroscopic and cytotoxicity studies of TbF3@CeF3 and TbF3@CeF3@SiO2 nanocrystals

Role of the CCL21 and CCR7 pathways in rheumatoid arthritis angiogenesis

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