9 research outputs found

    ALU element instability and cause-specific survival.

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    <p><b>(a, b)</b> CVD-associated percent survival of elderly adults predicted by <i>ALU-J/Sx</i> content over four years (<sup>★</sup><i>P</i> = 0.03; WBC-HR = 4.21, CI = 0.90–19.70; SMC-HR = 0.84, CI = 0.19–3.70), and <b>(c, d)</b> cancer-associated percent survival of elderly adults predicted by <i>ALU-J/Sx</i> content over four years (WBC-HR = 0.74, CI = 0.05–12.28; SMC-HR = 2.07, CI = 0.22–20.00). Terms—CVD: cardiovascular disease; <i>ALU-J/Sx</i> content: combined <i>ALU-J</i> and <i>ALU-Sx</i> content; WBC: white blood cells; SMC: smooth muscle cells; HR: hazard ratio; CI: confidence interval.</p

    D<sub>3</sub> blocks RHOA and ARF6 activation in destabilized endothelial cells.

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    <p>Endothelial cells were exposed to 10 μM D<sub>3</sub> or 7-DHC in combination with 2ng/mL TNF-α or IL-1β. Lysates were analyzed for RHOA-GTP and ARF6-GTP levels using appropriate precipitation assays. All graphs depict mean ± SEM. * denotes P<0.05, ** denotes P<0.01, and *** denotes P<0.001.</p

    D<sub>3</sub> stabilizes endothelial cells through a non-genomic mechanism.

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    <p><b>(A)</b> Endothelial cells were exposed to D<sub>3</sub> or its metabolites for 24 hours and lysates were probed for VDR transcription targets FOX01 and CYP24. Endothelial cells were exposed to D<sub>3</sub> or its metabolites in the presence of inhibitors of transcription (actinomycin D) and translation (cycloheximide) <b>(B, C)</b> and were assessed for transendothelial resistance or VDR target gene expression. All graphs depict mean ± SEM. * denotes P<0.05, and **** denotes P<0.0001. ### denotes P<0.001, and #### denotes P<0.0001 versus the respective control.</p

    D<sub>3</sub> abrogates inflammatory leak in culture and <i>ex</i> vivo.

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    <p>Monolayers of HMVEC were stimulated with D<sub>3</sub> (10 μM), 7-DHC(10 μM), or 0.5% DMSO (vehicle control) in the presence of inflammatory cytokines: IL-1β (10 ng/mL), TNF-α (2 ng/mL), and LPS (100 ng/mL) in an (<b>A-C</b>) ECIS or (<b>D</b>) transwell leak assay. (<b>E</b>) VEGF-induced leak of a fluorescent reporter in arterioles isolated from wild-type mice fed either standard chow or a D<sub>3</sub>-enhanced chow. All panels depict mean ± SEM. * denotes P<0.05, ** denotes P<0.01, and **** denotes P<0.0001.</p

    Vitamin D stabilizes the endothelium.

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    <p>Dose/time resistance (endothelial stability) surfaces generated with ECIS are shown from 100 pM to 10 μM and from zero to 21 hours for: (<b>A</b>) D<sub>3</sub>; (<b>F</b>) 25(OH)D<sub>3</sub>; (<b>K</b>) 1,25(OH)<sub>2</sub>D<sub>3</sub>. Detailed time-responses are shown at 1 nM and 10 μM respectively for: (<b>B</b> and <b>C)</b> D<sub>3</sub>; (<b>G</b> and <b>H</b>) 25(OH)D<sub>3</sub>; and (<b>L</b> and <b>M</b>) 1,25(OH)<sub>2</sub>D<sub>3</sub>. Detailed dose-response are shown at 4 hours and 12 hours respectively for (<b>D</b> and <b>E)</b> D<sub>3</sub>, (<b>I</b> and <b>J</b>) 25(OH)D<sub>3</sub>, and (<b>N</b> and <b>O</b>) 1,25(OH)<sub>2</sub>D<sub>3</sub>.</p

    Vitamin D sterol activity.

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    <p>Graphical models of the different vitamin D3 sterols, their metabolism, and a summary of their normal circulating levels, the minimum active dose for stabilizing the endothelium and doses in which the sterols have been reported to interact with vitamin D receptor [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0140370#pone.0140370.ref029" target="_blank">29</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0140370#pone.0140370.ref051" target="_blank">51</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0140370#pone.0140370.ref052" target="_blank">52</a>]. *Normal circulating levels vary upon many conditions including diet and UV exposure.</p

    D<sub>3</sub> promotes VE-cadherin cell-cell junction stability.

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    <p>(<b>A</b>) Endothelial cells were treated with TNF-α and either 7-DHC or D<sub>3</sub> for the denoted times and lysates were immunoblotted for p731 VE-cadherin or total VE-Cadherin. (<b>B</b>) Endothelial cell monolayers were exposed to the denoted pro-inflammatory cues in the presence of vehicle control, D<sub>3</sub> or 7DHC. Cells were fixed and VE-Cadherin was visualized through immunofluorescent labeling with automated image acquisition and analysis. All graphs depict mean ± SEM. * denotes P<0.05, ** denotes P<0.01, and *** denotes P<0.001.</p
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