Synergistic stimulation of alkaline phosphatase activity in bovine aortic endothelial cells grown in the presence of retinoids and glucocorticoids

Adams, Susan; Melnykovych, George

doi:10.1002/jcp.1041240119

Cited by 14 publications

(6 citation statements)

References 22 publications

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“…The study also revealed strongly down-regulated expression of the bone TNAP transcript when mouse BCECs were maintained in solo-culture for a few days [61]. Interestingly, a variety of molecules are known to modulate AP expression (retinoic acid [62]–[64]; cAMP [65]; glucocorticoids [62], [66]; transforming growth factor-beta [53]; IL-6 [53] and basic fibroblast growth factor [54], [67]) and brain capillary endothelial permeability. In the present study, we found that glial-cell-induced TNAP expression prevented a levamisole-induced increase in endothelial permeability - suggesting a protective effect.…”

Section: Discussionmentioning

confidence: 84%

TNAP and EHD1 Are Over-Expressed in Bovine Brain Capillary Endothelial Cells after the Re-Induction of Blood-Brain Barrier Properties

et al. 2012

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Although the physiological properties of the blood-brain barrier (BBB) are relatively well known, the phenotype of the component brain capillary endothelial cells (BCECs) has yet to be described in detail. Likewise, the molecular mechanisms that govern the establishment and maintenance of the BBB are largely unknown. Proteomics can be used to assess quantitative changes in protein levels and identify proteins involved in the molecular pathways responsible for cellular differentiation. Using the well-established in vitro BBB model developed in our laboratory, we performed a differential nano-LC MALDI-TOF/TOF-MS study of Triton X-100-soluble protein species from bovine BCECs displaying either limited BBB functions or BBB functions re-induced by glial cells. Due to the heterogeneity of the crude extract, we increased identification yields by applying a repeatable, reproducible fractionation process based on the proteins' relative hydrophobicity. We present proteomic and biochemical evidence to show that tissue non-specific alkaline phosphatase (TNAP) and Eps15 homology domain-containing protein 1(EDH1) are over-expressed by bovine BCECs after the re-induction of BBB properties. We discuss the impact of these findings on current knowledge of endothelial and BBB permeability.

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Section: Discussionmentioning

confidence: 84%

TNAP and EHD1 Are Over-Expressed in Bovine Brain Capillary Endothelial Cells after the Re-Induction of Blood-Brain Barrier Properties

et al. 2012

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“…Changes in the specific activity of alkaline phosphatase are not therefore due to a stimulation or inhibition of cell growth by these compounds. Adams and Melnykovych (1985) have shown that dexamethasone increased the alkaline phosphatase activity in bovine endothelial cells, but they concluded that the steroid was not acting via a receptor-mediated mechanism. In the LEII mouse endothelial cell line used in the …”

Section: Discussionmentioning

confidence: 95%

Recombinant human interleukin‐1 inhibits the induction by dexamethasone of alkaline phosphatase activity in murine capillary endothelial cells

Mulkins¹,

Allison²

1987

Journal Cellular Physiology

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A mutual antagonism exists between interleukin-1s (IL-1s) as pro-inflammatory and glucocorticoids as anti-inflammatory mediators. This report examines the effects of IL-1 on the induction by dexamethasone of alkaline phosphatase in LEII murine endothelial cells. Dexamethasone increases the specific activity of alkaline phosphatase in a time- and dose-dependent fashion (maximum 14-fold induction at 10(-6) M, IC50 = 10(-8) M), and this induction can be completely inhibited by simultaneous incubation with picomolar concentrations of recombinant human IL-1 alpha or IL-1 beta. This IL-1-mediated antagonism of dexamethasone activity is not due to a down-regulation of glucocorticoid receptors in the cell line used, because the number of receptors and their affinity for dexamethasone is unchanged in IL-1-treated cells. However, induction of alkaline phosphatase by dexamethasone in LEII cells is receptor-mediated, since it can also be inhibited by glucocorticoid-receptor antagonists.

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“…The study revealed strongly down-regulated expression of the bone TNAP transcript when mouse BCECs were maintained in solo-culture for a few days (Brun-Heath et al 2011). Interestingly, a variety of molecules are known to modulate TNAP expression [retinoic acid (Zhou et al 1994;Lechardeur et al 1995); cAMP (Beuckmann et al 1995); glucocorticoids (Adams and Melnykovych 1985;Mulkins and Allison 1987); transforming growth factor-beta (Nakazato et al 1997); IL-6 (Nakazato et al 1997) and basic fibroblast growth factor (Roux et al 1994;Sobue et al 1999)] (see also Chap. 4) and brain capillary endothelial permeability.…”

Section: Bbb-phenotype Induction By Surrounding Cellsmentioning

confidence: 91%

Tissue Non-specific Alkaline Phosphatase (TNAP) in Vessels of the Brain

Deracinois

Lenfant

Dehouck

et al. 2015

Subcellular Biochemistry

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The microvessels of the brain represent around 3-4 % of the brain compartment but constitute the most important length (400 miles) and surface of exchange (20 m(2)) between the blood and the parenchyma of brain. Under influence of surrounding tissues, the brain microvessel endothelium expresses a specific phenotype that regulates and restricts the entry of compounds and cells from blood to brain, and defined the so-called blood-brain barrier (BBB). Evidences that alkaline phosphatase (AP) is a characteristic feature of the BBB phenotype that allows differentiating capillary endothelial cells from brain to those of the periphery have rapidly emerge. Thenceforth, AP has been rapidly used as a biomarker of the blood-brain barrier phenotype. In fact, brain capillary endothelial cells (BCECs) express exclusively tissue non-specific alkaline phosphatase (TNAP). There are several lines of evidence in favour of an important role for TNAP in brain function. TNAP is thought to be responsible for the control of transport of some compounds across the plasma membrane of the BCECs. Here, we report that levamisole-mediated inhibition of TNAP provokes an increase of the permeability to Lucifer Yellow of the endothelial monolayer. Moreover, we illustrate the disruption of the cytoskeleton organization. Interestingly, all observed effects were reversible 24 h after levamisole removal and correlated with the return of a full activity of the TNAP. This reversible effect remains to be studied in details to evaluate the potentiality of a levamisole treatment to enhance the entry of drugs in the brain parenchyma.

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Synergistic stimulation of alkaline phosphatase activity in bovine aortic endothelial cells grown in the presence of retinoids and glucocorticoids

Cited by 14 publications

References 22 publications

TNAP and EHD1 Are Over-Expressed in Bovine Brain Capillary Endothelial Cells after the Re-Induction of Blood-Brain Barrier Properties

TNAP and EHD1 Are Over-Expressed in Bovine Brain Capillary Endothelial Cells after the Re-Induction of Blood-Brain Barrier Properties

Recombinant human interleukin‐1 inhibits the induction by dexamethasone of alkaline phosphatase activity in murine capillary endothelial cells

Tissue Non-specific Alkaline Phosphatase (TNAP) in Vessels of the Brain

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