Multi-wavelength Stellar Polarimetry of the Filamentary Cloud IC5146: I. Dust Properties

We present optical and near-infrared stellar polarization observations toward the dark filamentary clouds associated with IC5146. The data allow us to investigate the dust properties (this paper) and the magnetic field structure (Paper II). A total of 2022 background stars were detected in $R_{c}$-, $i'$-, $H$-, and/or $K$-bands to $A_V \lesssim 25$ mag. The ratio of the polarization percentage at different wavelengths provides an estimate of $\lambda_{max}$, the wavelength of peak polarization, which is an indicator of the small-size cutoff of the grain size distribution. The grain size distribution seems to significantly change at $A_V \sim$ 3 mag, where both the average and dispersion of $P_{R_c}/P_{H}$ decrease. In addition, we found $\lambda_{max}$ $\sim$ 0.6-0.9 $\mu$m for $A_V>2.5$ mag, which is larger than the $\sim$ 0.55 $\mu$m in the general ISM, suggesting that grain growth has already started in low $A_V$ regions. Our data also reveal that polarization efficiency (PE $\equiv P_{\lambda}/A_V$) decreases with $A_V$ as a power-law in $R_c$-, $i'$-, and $K$-bands with indices of -0.71$\pm$0.10, -1.23$\pm$0.10 and -0.53$\pm$0.09. However, $H$-band data show a power index change; the PE varies with $A_V$ steeply (index of -0.95$\pm$0.30) when $A_V < 2.88\pm0.67$ mag but softly (index of -0.25$\pm$0.06) for greater $A_V$ values. The soft decay of PE in high $A_V$ regions is consistent with the Radiative Aligned Torque model, suggesting that our data trace the magnetic field to $A_V \sim 20$ mag. Furthermore, the breakpoint found in $H$-band is similar to the $A_V$ where we found the $P_{R_c}/P_{H}$ dispersion significantly decreased. Therefore, the flat PE-$A_V$ in high $A_V$ regions implies that the power index changes result from additional grain growth.Comment: 31 pages, 17 figures, and 3 tables; accepted for publication in Ap

D₃ blocks RHOA and ARF6 activation in destabilized endothelial cells.

<p>Endothelial cells were exposed to 10 μM D₃ 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

Vitamin D sterol activity.

<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

D₃ stabilizes endothelial cells through a non-genomic mechanism.

<p><b>(A)</b> Endothelial cells were exposed to D₃ or its metabolites for 24 hours and lysates were probed for VDR transcription targets FOX01 and CYP24. Endothelial cells were exposed to D₃ 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

D₃ abrogates inflammatory leak in culture and <i>ex</i> vivo.

<p>Monolayers of HMVEC were stimulated with D₃ (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 D₃-enhanced chow. All panels depict mean ± SEM. * denotes P<0.05, ** denotes P<0.01, and **** denotes P<0.0001.</p

D₃ promotes VE-cadherin cell-cell junction stability.

<p>(<b>A</b>) Endothelial cells were treated with TNF-α and either 7-DHC or D₃ 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, D₃ 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

Vitamin D stabilizes the endothelium.

<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>) D₃; (<b>F</b>) 25(OH)D₃; (<b>K</b>) 1,25(OH)₂D₃. Detailed time-responses are shown at 1 nM and 10 μM respectively for: (<b>B</b> and <b>C)</b> D₃; (<b>G</b> and <b>H</b>) 25(OH)D₃; and (<b>L</b> and <b>M</b>) 1,25(OH)₂D₃. Detailed dose-response are shown at 4 hours and 12 hours respectively for (<b>D</b> and <b>E)</b> D₃, (<b>I</b> and <b>J</b>) 25(OH)D₃, and (<b>N</b> and <b>O</b>) 1,25(OH)₂D₃.</p