Novel mouse endothelial cell surface marker is suppressed during differentiation of the blood brain barrier

Hallmann, Rupert; Mayer, D. N.; Berg, Ellen L.; Broermann, R.; Butcher, Eugene C.

doi:10.1002/aja.1002020402

Cited by 196 publications

(157 citation statements)

References 22 publications

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“…29,30 Furthermore, in our coculture system, the expression of occludin, claudin-5, claudin-3 and JAM-1 and peripheral distribution of these proteins suggested the well differentiation of tight junctions. However, claudin-1 was not detected.…”

Section: Discussionmentioning

confidence: 60%

Mouse syngenic in vitro blood–brain barrier model: a new tool to examine inflammatory events in cerebral endothelium

Coisne

Dehouck

Faveeuw

et al. 2005

Laboratory Investigation

165

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Although cerebral endothelium disturbance is commonly observed in central nervous system (CNS) inflammatory pathologies, neither the cause of this phenomenon nor the effective participation of bloodbrain barrier (BBB) in such diseases are well established. Observations were mostly made in vivo using mouse models of chronic inflammation. This paper presents a new mouse in vitro model suitable for the study of underlying mechanistic events touching BBB functions during CNS inflammatory disturbances. This model consists of a coculture with both primary cell types isolated from mice. Mouse brain capillary endothelial cell (MBCEC)s coming from brain capillaries are in culture with their in vivo partners and form differentiated monolayers that retain endothelial markers and numerous phenotypic properties of in vivo cerebral endothelium, such as: (1) Keywords: BBB; in vitro model; coculture; tight junction; P-glycoprotein; cell adhesion moleculeThe maintenance of brain interstitial fluid homeostasis is established by the presence of the bloodbrain barrier (BBB) which can be considered as the main interface between blood and brain parenchymal cells. This endothelium can be distinguished from the other vascular beds by the presence of continuous tight junctions and the absence of fenestration or channel. Both of these characteristics reduce the unspecific transport of molecules across the BBB. The blood/brain exchanges involve specific carrier-mediated transport systems that facilitate the uptake of nutrients. 1,2 BBB damage commonly associated to inflammatory events has been reported in several central nervous system (CNS) infections and neurodegenerative diseases. [3][4][5] Although BBB permeability disturbances seem to be critical steps as they lead to brain damage, neither the cause of these phenomena nor the effective participation of BBB in such diseases are established.The cerebral vascular wall was formally considered as a barrier that isolates brain from immunecontrol. However, the presence of immune cells in the brain parenchyma in healthy animals, and their increased cerebral residence in pathogenic conditions, demonstrate that the recruitment of inflammatory cells into the CNS, through the BBB, takes place. 6,7 In fact, the presence of cell adhesion molecules (CAMs) on the BBB suggests a direct and selective interaction between blood cells and the cerebral endothelium. These molecules, first described in peripheral capillaries, may mediate leukocyte transmigration across the BBB in a multistep process. 8,9 BBB damages and leukocyte infiltration in brain parenchyma were mostly examined using in vivo mouse models of chronic inflammation, which are

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Section: Discussionmentioning

confidence: 60%

Mouse syngenic in vitro blood–brain barrier model: a new tool to examine inflammatory events in cerebral endothelium

Coisne

Dehouck

Faveeuw

et al. 2005

Laboratory Investigation

165

View full text Add to dashboard Cite

show abstract

“…10 Antibodies used for immunohistochemistry include monoclonal rat anti-mouse macrophage antibodies F4/80 (MCA497R, Serotec, Raleigh, NC) and rat anti-Mac-3 (clone M3/84, BD Biosciences, San Diego, CA), goat anti-PCNA antibody (sc-9857, Santa Cruz Biotechnology, Santa Cruz, CA) rabbit anti-active caspase 3 (AF835, R&D Systems, Minneapolis, MN), and monoclonal rat anti-mouse endothelial cell antibody MECA 32 13 (DSHB, University of Iowa, Iowa City, IA). Immunohistochemistry on acetone fixed frozen sections was performed and quantified as described.…”

Section: Antibodiesmentioning

confidence: 99%

Combination of a monoclonal anti‐phosphatidylserine antibody with gemcitabine strongly inhibits the growth and metastasis of orthotopic pancreatic tumors in mice

Beck

Luster

Miller

et al. 2006

Intl Journal of Cancer

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Pancreatic cancer continues to have a dismal prognosis and novel therapy is needed. In this study, we evaluate a promising new target for therapy, phosphatidylserine (PS). PS is an anionic phospholipid located normally on the inner leaflet of the plasma membrane in mammalian cells. In the tumor microenvironment, PS becomes externalized on vascular endothelium. The monoclonal antibody 3G4 binds PS and promotes an inflammatory response against tumor blood vessels, resulting in reduction of tumor growth. Mice with orthotopic pancreatic tumors were treated with 3G4, gemcitabine or a combination of both drugs. Tumor burden including pancreas weight and metastatic lesions (liver, lymph node and peritoneal) were reduced 3-to 5-fold by the combination therapy as compared with 1.5-to 2-fold with 3G4 and gemcitabine alone, respectively. Treatment of tumor-bearing animals with the combination therapy increased macrophage infiltration into the tumor mass 10-fold and reduced microvessel density in the tumor by 2.5-fold compared with tumors from untreated animals. Gemcitabine alone and 3G4 alone were less effective than the combination of the 2 agents together. The additive therapeutic effect of both agents appears to be because chemotherapy increases PS exposure on tumor vascular endothelium and amplifies the target for attack by 3G4. In conclusion, 3G4 enhanced the anti-tumor and anti-metastatic activity of gemcitabine without contributing to toxicity. ' 2005 Wiley-Liss, Inc.

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“…11 The microvessel density (MVD) was determined as previously described. 12 To assess the proliferative index, immunostaining for Ki-67 was used.…”

Section: Histology Immunohistochemistry and In Situ Cell Death Detecmentioning

confidence: 99%

Activation of FGFR1β signaling pathway promotes survival, migration and resistance to chemotherapy in acute myeloid leukemia cells

et al. 2006

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Fibroblast growth factors (FGFs) are important regulators of hematopoiesis and have been implicated in the tumorigenesis of solid tumors. Recent evidence suggests that FGF signaling through FGF receptors (FGFRs) may play a role in the proliferation of subsets of acute myeloid leukemias (AMLs). However, the precise mechanism and specific FGF receptors that support leukemic cell growth are not known. We show that FGF-2, through activation of FGFR1b signaling, promotes survival, proliferation and migration of AML cells. Stimulation of FGFR1b results in phosphoinositide 3-kinase (PI3-K)/Akt activation and inhibits chemotherapy-induced apoptosis of leukemic cells. Neutralizing FGFR1-specific antibody abrogates the physiologic and chemoprotective effects of FGF-2/FGFR1b signaling and inhibits tumor growth in mice xenotransplanted with human AML. These data suggest that activation of FGF-2/ FGFR1b supports progression and chemoresistance in subsets of AML. Therefore, FGFR1 targeting may be of therapeutic benefit in subsets of AML. Leukemia (2006) 20, 979-986.

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Novel mouse endothelial cell surface marker is suppressed during differentiation of the blood brain barrier

Cited by 196 publications

References 22 publications

Mouse syngenic in vitro blood–brain barrier model: a new tool to examine inflammatory events in cerebral endothelium

Mouse syngenic in vitro blood–brain barrier model: a new tool to examine inflammatory events in cerebral endothelium

Combination of a monoclonal anti‐phosphatidylserine antibody with gemcitabine strongly inhibits the growth and metastasis of orthotopic pancreatic tumors in mice

Activation of FGFR1β signaling pathway promotes survival, migration and resistance to chemotherapy in acute myeloid leukemia cells

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