1,724,893 research outputs found
Overexpression of miR-4516 inhibited the PVR progression in vivo.
No full text(A) 0.1 mL of TGF-β2 (10 ng/mL) and 0.1 mL of balanced salt solution containing approximately 1 × 106 miR-4516 and ARPE-19 cells transfected with miR-negative control (NC) were injected into the right eyes. A total of four doses was administered to each eye on days 1, 8, 15, and 22. PVR progression was determined according to the Fastenberg classification (stages 1–5) at day 37 post-injection. (B) Results from the independent samples U test of differences in PVR stage between the control group and the miR-4516-treated group. (C) Ultrasonic examination of the control eye and the miR-4516-treated eye at day 37 post-injection. (D) Hematoxylin and eosin staining revealed the presence of dense fibrovascular membrane tissue and considerably higher infiltration of inflammatory cells on the retinal surface of eyes treated with miR-NC compared with that of eyes treated with miR-4516. *p<0.05; **p<0.01.</p
Transdifferentiationin RPE cells was inhibited by miR-4516 delivery.
No full text(A) The expression levels of miR-4516 in ARPE-19 cells transfected with negative control or a miR-4516 mimic, as determined through real-time quantitative polymerase chain reaction. ***p<0.001. (B) Morphologic alterations in ARPE-19 cells transfected with negative control or miR-4516 and incubated in the presence or absence of TGF-β2 (10 ng/mL). The cells were examined by phase-contrast microscopy.</p
Expression of miR-4516 was suppressed by TGF-β2.
No full text(A) Expression of miR-4516 and others in ARPE-19 cells. (B) MiR-4516 expression in ARPE-19 cells treated with or without transforming growth factor (TGF)-β1, TGF-β2, total TGF-β, IFN-γ, and TNF-α (10 ng/mL) for 24 hours. The expression levels of miR-4516 were normalized to those of the control, U6 small nuclear RNA. Data are presented as the means ± standard errors of the mean of three replicates. *p< 0.05; **p<0.01.</p
Block Card 4516 Glendale Avenue
No full textThis image was produced by the Auditor's Office in Lucas County, Ohio for tax assessment purposes. Associated dates are approximate. Descriptive terms related to this photograph include: Cape Cod Style | 4516 Glendale Avenue (Toledo, Ohio) | Dwelling | South Toledo Area (Toledo, Ohio
The infrared counterpart and proper motion of magnetar SGR0501+4516
Get PDFInternational audienceSoft gamma repeaters (SGRs) are highly magnetised neutron stars (magnetars) notable for their gamma-ray and X-ray outbursts. In this paper, we use near-infrared (NIR) imaging of SGR 0501+4516 in the days, weeks, and years after its 2008 outburst to characterise the multi-wavelength emission, and to obtain a proper motion from our long temporal baseline observations. Unlike most magnetars, the source has only moderate foreground extinction with minimal crowding. Our observations began only 2 hours after the first activation of SGR 0501+4516 in August 2008, and continued for 4 years, including two epochs of Hubble Space Telescope (HST) imaging. The proper motion constraint is improved by a third HST epoch 10 years later. The near-infrared and X-rays faded slowly during the first week, thereafter following a steeper power-law decay. The behaviour is satisfactorily fit by a broken power-law. Three epochs of HST imaging with a 10-year baseline allow us to determine a quiescent level, and to measure a proper motion of 5.4+/-0.6 mas/yr. This corresponds to a low transverse peculiar velocity of 51+/-14 km/s (at 2 kpc). The magnitude and direction of the proper motion rules out supernova remnant HB9 as the birth-site. We can find no other supernova remnants or groups of massive stars within the region traversed by SGR 0501+4516 during its characteristic lifetime (20 kyr). Our observations of SGR 0501+4516 suggest that some magnetars may be either significantly older than expected, that their progenitors produce low supernova ejecta masses, or alternatively that they can be formed through accretion-induced collapse (AIC) or low-mass neutron star mergers. Although the progenitor of SGR 0501+4516 remains unclear, we propose that SGR 0501+4516 is the best Galactic candidate for a magnetar formed through a mechanism other than massive star core-collapse
Block Card 4516 McKain Drive
No full textThis image was produced by the Auditor's Office in Lucas County, Ohio for tax assessment purposes. Associated dates are approximate. Descriptive terms related to this photograph include: Ranch houses | 4516 McKain Drive (Toledo, Ohio) | Dwelling | Greenbush Knolls Addition (Toledo, Ohio) | Trilby Area (Toledo, Ohio)
Block Card 4516 Monac Drive
No full textThis image was produced by the Auditor's Office in Lucas County, Ohio for tax assessment purposes. Associated dates are approximate. Descriptive terms related to this photograph include: Ranch houses | 4516 Monac Drive (Toledo, Ohio) | Dwelling | Greenbush Knolls Addition (Toledo, Ohio) | Trilby Area (Toledo, Ohio)
PVR was inhibited by miR-4516 overexpression in vitro.
No full text(A) ARPE-19 cells were pre-transfected with negative control or the miR-4516 mimic for 24 hours and then treated with TGF-β2 (10 ng/mL) in the presence or absence of the miR-4516 mimic for 3 days. (B) Contraction or expansion was determined as a percentage of the original area. Results are presented as means ± standard errors of the mean of three independent experiments. *p<0.05; **p<0.01; ns: not significant.</p
Abstract 5726: A novel tumor-promoting role for miR-4516 in glioblastoma
No full textAbstract
Background: Glioblastomas are the most aggressive high-grade brain tumors, which are often life-threatening due to their location and rapid growth. Although survival rates differ depending on a variety of genetic and environmental factors, the average survival rate for a glioblastoma (GBM) patient is less than 15 months. Although the mechanisms of tumorigenesis are still being elucidated, miRNAs are promising candidates to explore as novel and prognostic biomarkers in GBM. Here we demonstrate a novel role for miR-4516 in promoting growth and migration of GBM and establish the molecular mechanisms mediating these functions. Methods: Formalin-fixed, paraffin-embedded tissue blocks (n=268) were collected for all patients and total RNA was isolated. miRNAs were analyzed simultaneously using the nCounter human miRNA v2 assay (NanoString Technologies; Seattle,WA). Functional characterization studies were conducted in vitro and in vivo. The effect of miR-4516 on GBM cell growth and motility were evaluated by cell proliferation assay, migration and invasion assay, and Annexin-V assay. Realtime PCR, immunoblotting, and 3’ untranslated region luciferase assays were used to analyze miR-4516 targets and signaling pathways. Intracranial injection will be performed to investigate the role of miR-4516 in tumor growth in vivo. Results: Univariate analysis showed that miR-4516 expression in GBM patients was inversely correlated with overall survival (FDR=0.002, p=1.02E-05). Knockdown of miR-4516 blocked tumor growth and induced cell apoptosis. Tumor cell growth, migration and invasion were induced in both transient miR-4516 overexpressed GBM cells (LN229, LN18, and U87) and stable miR-4516 overexpressed GBM cells (U87-EGFRvIII). These miR-4516 tumor-promoting effects were mediated in part via direct targeting PTPN14 and CDKN1A. Investigation of the other miR-4516 targets and in vivo functional study are in process. Conclusion: Taken together, these results suggest that miR-4516 acts as a prognostic biomarker for GBM patients. Funding Information: 1R01CA169368 (PI: Houghton; Co-I:Chakravarti); 1R01CA11522358 Multiple-PI R01: Chakravarti (PI); Xia (PI); 1R01CA1145128 Baroukhim (PI); Chakravarti (Co-PI) 7/2015-6/2020; R01CA108633 (PI:Chakravarti); 1RC2CA148190 (Scientific PI: Chakravarti)
Citation Format: Tiantian Cui, Ashley Gray, Ziyan Liu, Marjolein Geurts, Pierre Robe, Joseph McElroy, Erica Hlavin Bell, Arnab Chakravarti. A novel tumor-promoting role for miR-4516 in glioblastoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5726. doi:10.1158/1538-7445.AM2017-5726</jats:p
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