12 research outputs found

    The expression levels and correlation of miR-5195-3p and GMFB.

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    (A) In HG-induced ARPE-19 cells, miR-5195-3p was significantly downregulated compared with that of NG group. (B) GMFB protein expression was upregulated in HG-induced ARPE-19 cells compared with that of NG group. ***p p < 0.01 compared with miR-NC. NC, negative control; HG, high glucose; NG, normal glucose; WT, wild type; MUT, mutant type.</p

    Effects of miR-5195-3p overexpression on ARPE-19 cell viability, inflammation and apoptosis after HG stimulation.

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    (A) Analysis of reverse transcription quantitative PCR was conducted to evaluate miR-5195-3p expression in ARPE-19 cells transfected with miR-5195-3p mimics or miR-NC. ***p p p p < 0.01, compared with HG + miR-NC; NC, negative control; HG, high glucose; NG, normal glucose.</p

    Overexpression of GMFB reversed the protective effects of miR-5195-3p overexpression against HG-induced ARPE-19 cell injury.

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    ARPE-19 cells were co-transfected with miR-5195-3p mimics with either pcDNA3.1-GMFB or pcDNA3.1, followed by 24 h incubation with HG. (A) The protein expression of GMFB was detected by western blot analysis. (B) Cell viability was analyzed using CCK-8 assay. (C-D) ELISA assay was performed to analyze the release of IL-1β and TNF-α in transfected ARPE-19 cells, followed by HG stimulation. (E) The percentages of apoptotic cells were compared in transfected ARPE-19 cells, followed by HG stimulation. Data were shown as mean ± SD. *p p p p p < 0.001, compared with HG + miR-5195-3p mimics + pcDNA3.1; NC, negative control; HG, high glucose.</p

    Knockdown of GMFB enhanced the protective effects of miR-5195-3p overexpression against HG-induced ARPE-19 cell injury.

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    ARPE-19 cells were co-transfected with miR-5195-3p mimics and si-GMFB or si-NC, and then treated with HG for 24 h. (A) The protein expression of GMFB was detected by western blot analysis. (B) Cell viability was analyzed using CCK-8 assay. (C-D) ELISA assay was performed to analyze the release of IL-1β and TNF-α in transfected ARPE-19 cells, followed by HG stimulation. (E) The percentages of apoptotic cells were compared in transfected ARPE-19 cells, followed by HG stimulation. Data were shown as mean ± SD. *p p p p < 0.01, compared with HG + miR-5195-3p mimics + si-NC; NC, negative control; HG, high glucose; si, small interfering.</p

    Effects of GMFB knockdown on ARPE-19 cell viability, inflammation and apoptosis after HG stimulation.

    No full text
    (A) Western blot analysis was conducted to evaluate GMFB protein expression in ARPE-19 cells transfected with si-GMFB or si-NC. (B) The transfected ARPE-19 cells were exposed to HG, followed by CCK-8 assay. (C) ELISA assay was performed to analyze the release of IL-1β and TNF-α in transfected ARPE-19 cells, followed by HG stimulation. (D) The percentages of apoptotic cells were compared in transfected ARPE-19 cells, followed by HG stimulation. Data were shown as mean ± SD. **p p p p < 0.01, compared with HG + si-NC; NC, negative control; HG, high glucose; NG, normal glucose; si, small interfering.</p

    MOESM2 of Effect of cytoglobin overexpression on extracellular matrix component synthesis in human tenon fibroblasts

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    Additional file 2: Fig. S1. Immunostaining in Cygb overexpression group and control group. Intracellular protein signal was detectable in Cygb overexpression group but not in control group

    Phthalimide-Carried Disulfur Transfer To Synthesize Unsymmetrical Disulfanes via Copper Catalysis

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    A versatile Cu-catalyzed cross-coupling reaction to various unsymmetrical disulfanes has been presented, from phthalimide-carried disulfur transfer reagents and commercially available boronic acids under mild and practical conditions. The method features the unprecedented use of phthalimide-carried disulfurating reagents (Harpp reagent) in cross-coupling chemistry and is highlighted by the broad substrate scopes, even applicable for the transfer of aryl-disulfur moieties (ArSS−). Notably, the robustness of this methodology is shown by the late-stage modification of bioactive scaffolds of coumarin, estrone, and captopril
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