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

    Effect of SILD on STZ-diabetic kidney: modulation of macrophage infiltration.

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    <p>(A) Representative photomicrographs of H&E-stained kidneys (×200 magnification) on harvesting show normal structure in the CTRL and SILD, mild mesangial expansion and tubular damage in the STZ, and normal structure in the STZ+SILD group (bar represents 100 μm).(B) and (C) Glomerular and tubulointerstitial damage index scores are shown for each group. Data are expressed as mean ± SD. <sup><b>**</b></sup>P <0.01 STZ vs CTRL; <sup><b>##</b></sup>P <0.01 vs STZ (Student’s t-test).(D) Histograms indicate percentage of F4/80<sup><b>+</b></sup> cells. Results are expressed as mean ± SD (n = 4 in each group) <sup><b>**</b></sup>P <0.01 STZ vs CTRL; <sup><b>##</b></sup>P <0.01 STZ+SILD vs STZ (Student’s t-test).(E) Immunophenotype of infiltrating macrophages in kidneys from representative CTRL, SILD, STZ and STZ+SILD mice, performed to assess expression of F4/80 and CD11b. Percentage of F4/80<sup><b>+</b></sup> cells is augmented in STZ mice. One experiment representative of several independent experiments is shown.(F) Confocal analysis for F4/80 (green) and iNOS (red) shows abundant interstitial inflammatory macrophages (iNOS<sup><b>+</b></sup>) in renal sections from STZ mice, that were significantly decreased in STZ+SILD mice. (G) Relative F4/80<sup><b>+</b></sup> and iNOS<sup><b>+</b></sup> area quantification. Each dot represents one slide in different kidney groups.(H) Quantification of VCAM-1 and COX-2 to GAPDH expression detected by Western blotting reveals vascular inflammation in kidneys from STZ mice and less damage in kidneys from STZ+SILD mice.</p

    Metabolic characteristics and survival of treated mice.

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    <p>(A) Schematic representation of the experimental design. (B) Plasma glucose levels in diabetic (STZ and STZ+SILD) vs. non-diabetic (CTRL) mice. Results are expressed as mean ± SD (n = 7 in each group). (C) Changes in water consumption in STZ and STZ+SILD vs. CTRL mice. Results are expressed as mean ± SD (n = 4 in each group). (D) Changes in food consumption index in STZ and STZ+SILD vs. CTRL mice. Results are expressed as mean ± SD (n = 4 in each group). (E) Kaplan-Meier survival curve of CTRL, SILD, STZ and STZ+SILD mice.</p

    Mice group characteristics after 3-week sildenafil treatment.

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    <p>Values are presented as mean ± SD, <sup>a</sup>P <0.05 and <sup>aa</sup>P <0.01, STZ treated versus normal and <sup>b</sup>P<0.05, STZ+SILD treated versus STZ.</p><p>Mice group characteristics after 3-week sildenafil treatment.</p

    Effect of SILD on cardiac hypertrophy and macrophage infiltration.

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    <p>(A) Representative photomicrographs of H&E-stained heart from CTRL, SILD, STZ and STZ+SILD mice on harvesting (bar represents 100μm).(B) Histogram shows heart cross-sectional area. Results are expressed as mean ± SD (n = 4 in each group). <sup>*</sup>P <0.05 STZ vs CTRL; <sup>#</sup>P <0.05 STZ+SILD vs STZ (Student’s t-test).(C) Histogram shows mRNA quantitative analysis ANP. Results are expressed as mean ± SD (n = 3 in each group). <sup>*</sup>P <0.05 STZ vs CTRL; <sup>##</sup>P <0.01 STZ+SILD vs STZ (Student’s t-test).(D) β-MHC and GAPDH expression detected by Western blotting. Histogram shows activation of hypertrophic protein in STZ mice that was reduced in STZ+SILD mice. Results are expressed as mean ± SD (n = 3 in each group) <sup>##</sup>P <0.01 STZ+SILD vs STZ (Student’s t-test).(E) Histogram illustrates percentage of infiltrating F4/80<sup>+</sup> cells in the heart from CTRL, SILD, STZ and STZ+SILD mice. Results are expressed as mean ± SD (n = 4 in each group). <sup>*</sup>P <0.05 STZ vs CTRL; <sup>#</sup>P <0.0 STZ+SILD vs STZ (Student’s t-test).(F) Histograms indicates percentage of F4/80<sup>+</sup>TIE2<sup>+</sup> cells. Expression of F4/80<sup>+</sup>TIE2<sup>+</sup> cells was decreased in STZ compared with CTRL mice and increased in STZ+SILD compared with STZ mice. Results are expressed as mean ± SD (n = 4 in each group), <sup>*</sup>P <0.05 STZ vs CTRL; <sup>##</sup>P <0.01 STZ+SILD vs STZ (Student’s t-test).(G) iNOS and COX-2 expression detected by Western blotting. Histogram shows induction of inflammatory proteins in STZ mice that was reduced in STZ+SILD mice. Results are expressed as mean ± SD (n = 3 in each group). <sup>**</sup>P <0.01 STZ vs CTRL, <sup>##</sup>P <0.01 STZ+SILD vs STZ (Student’s t-test).</p

    SILD increases renal expression of TEMs pro-angiogenic macrophages.

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    <p>(A) Representative of at least 4 flow cytometry analyses of macrophage infiltration in kidney from CTRL, SILD, STZ and STZ+SILD mice, showing TIE2 expression in a subset of monocytes (filled line in the histogram plots).(B) Histograms indicate percentage of TIE2<sup><b>+</b></sup> in the F4/80<sup><b>+</b></sup> macrophages population. Expression of F4/80<sup><b>+</b></sup>TIE2<sup><b>+</b></sup> cells decreased in STZ compared to CTRL mice and increased in the STZ+SILD compared to STZ mice. Results are expressed as mean ± SD (n = 4 in each group); <sup><b>*</b></sup>P <0.01 STZ vs CTRL; <sup><b>##</b></sup>P <0.01 STZ+SILD vs STZ (Student’s t-test).(C) Confocal analysis for kidney TEMs from representative CTRL, SILD, STZ and STZ+SILD mice, performed for TIE2 (green) and MRC1 (blu). TIE2<sup><b>+</b></sup>MRC1<sup><b>+</b></sup> macrophages were lower in STZ than in CTRL and higher in SILD and STZ+SILD groups (bar represents 30μm).</p

    SILD inhibits high-glucose-induced adhesion via TIE2 receptor.

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    <p>(A) THP1 cell adhesion to HUVEC. Note that there are more adherent monocyte cells in high-glucose than in normal condition medium. SILD inhibits high-glucose-induced adhesion and co-treatment with TIE2-Fc cancelled this effect (n = 3/treatment group). (B) Quantification of monocyte adhesion to HUVEC. Histogram shows number of adherent cells per field in different experimental groups (n = 3/group). Results are shown as mean ± SD (n = 5 in each group). <sup><b>***</b></sup> P <0.001. <sup><b>**</b></sup> P <0.01 (Student’s t-test).(C) VCAM-1, NF-kB and GAPDH expression detected by Western blotting reveals that SILD inhibits vascular inflammation induced by high glucose treated HUVEC, while co-treatment TIE2-Fc cancelled this effect in VCAM-1.</p
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