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Decidual Endothelial Cells (DEC) and endothelial cells from human skin (ADMEC)

ABSTRACT: BACKGROUND: endothelial cells (ECs) form a continuous barrier between blood and tissues and gate the traffic of molecules and cells across the vessel wall playing an active role in hemostasis, inflammation and immunity. Decidual endothelial cells (DECs) are located in a very special district from the immunological and inflammatory point of view since decidua has immunoregulatory and pro-angiogenic functions. The aim of this study was to compare the phenotype of microvascular ECs isolated from decidua with microvascular ECs isolated from other vascular districts. METHOD: we analyzed the differences in molecules involved in angiogenesis and leukocyte recruitment between DECs and endothelial cells from human skin (ADMECs) which are normally involved in inflammatory response by microarray analysis. RESULTS: our results showed that DECs are able to produce high amount of the growth factors HGF, VEGF-A and IGFBP3, important for the control of angiogenesis and express the adhesion molecules ICAM2 and ICAM3 in basal condition, important molecules for the control of leukocyte recruitment and function. We demonstrated also that DECs do not up-regulate the expression of ICAM1 in response to pro-inflammatory cytokines and produce high amount of the chemokines CXCL9/MIG and CXCL10/IP-10 in response to IFN-a. CONCLUSION: we conclude that the phenotype of these cells strongly differs from that of other endothelial cells such as ADMECs which have to be quickly able to response to infections and other pro-inflammatory stimuli. These data suggest that endothelial cells may play an active in the control of local immune response at foeto-maternal interface.

ORGANISM(S): Homo sapiens

PROVIDER: GSE41946 | GEO | 2013/02/01

SECONDARY ACCESSION(S): PRJNA178566

REPOSITORIES: GEO

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Project description:The blood-brain barrier (BBB) dynamically controls and maintains a precisely balanced brain microenvironment necessary for reliable functioning. It is made up of highly specialized endothelial cells (ECs) in the lining of the vascular wall. These ECs are surrounded by the basal lamina, astrocytic perivascular endfeet, pericytes, microglia and neuronal processes that have been shown to contribute to barrier function1. In essence, the brain endothelium limits both transcellular and paracellular passage of cells and molecules into the central nervous system (CNS). Transcellular passage of hydrophilic molecules is limited due to a low rate of transcytotic vesicles, an extremely low pinocytotic activity, expression of active efflux transporters, and high metabolic activity. Paracellular diffusion of hydrophilic molecules and trafficking of immune cells is restricted by a network of tight junctions (TJs)2-5. Due to these characteristics, the BBB is able to protect the CNS from sudden changes in blood composition and uncontrolled influx of immune cells. In a large number of neuro-inflammatory diseases, an impaired function and an opening of the BBB are observed. In diseases of the CNS like multiple sclerosis or stroke or after brain trauma, the BBB becomes inflamed (mediated by for example reactive oxygen species (ROS) and hypoxia) and its function severely impaired which gives rise to enhanced cellular infiltration, thus contributing to tissue damage and neurological deficits. Due to the specialized nature of brain ECs, transmigration of leukocytes through cerebrovascular endothelium is likely to differ from that in other vascular beds. Generally, the transmigration process is closely controlled by the interaction of leukocytes with the endothelial surface followed by low velocity rolling, arrest, firm adhesion, and finally transmigration. For the diapedesis of immune cells across the cerebral vasculature a re-arrangement of the cytoskeleton and opening of the TJ complexes is required to allow cells to pass into the sub endothelial space. In the initial step of the adhesive cascade leukocytes adhere to the endothelium with low affinity. This adhesion is mediated by several members of the selectin family and their corresponding ligands. Despite the low affinity of these interactions, resulting contact of leukocytes with the endothelium leads to further activation of both cell types and finally transmigration of the leukocytes through the BBB6,7. The glycosylation of endothelial cells of different vascular bed origins To date it is unknown which specific carbohydrate structures on the BBB endothelium mediate leukocyte capture and rolling, and whether these structures are differentially expressed onto inflamed brain EC compared to normal brain ECs and vascular beds of other organs. Initial studies using qPCR and FACS analysis within our group reveal that brain endothelial cells have a different profile in their glycosylation-related genes compared to microvascular ECs upon inflammation, which may result in a different glycosylation profile of adhesive structures and may underlie rolling, adhesion and diapedesis of leukocytes. In this project we wish to identify specific, glycosylated structures on brain endothelial cells that mediate capture, rolling and diapedesis of leukocytes in the brain. To investigate the expression of glycosyltransferases in dendritic cells and the changes in expression associated with maturation. RNA preparations from stimulated and non-stimulated hcMEC/D3 (human brain endothelial cells line) and FMVEC (human promary microvascular endothelial cells isolated from foreskins) were sent to both Microarray Core (E) and Core(C). The RNA was put on an RNeasy Column, amplified, labeled, and hybridized to the Glycov3 microarrays. Data was sent to Dr. van Kooyk's lab for analysis.

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Decidual Endothelial Cells (DEC) and endothelial cells from human skin (ADMEC)

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