Fig 1: Accumulative cytotoxic effect of doxorubicin and tumor cells on HUVECs. Representative fluorescent images of actin filaments (phalloidin, green fluorescence) showing morphology of endothelial cells stimulated by different concentrations of doxorubicin as well as MCF7 cells for 24 h at low (A) and high magnifications (B). Representative immunofluorescent images of ICAM1 (red fluorescence) of HUVECs stimulated by different concentrations of doxorubicin as well as MCF7 cells for 24 h at low (C) and high magnifications (D). Representative immunofluorescent images of THP1 (orange fluorescence) and endothelial cell (green fluorescence) adhesion stimulated by different concentrations of doxorubicin in the presence of MCF7 cells at high magnifications (E). Quantitation of cell numbers per view is measured and presented in panel (F). Quantitation of mean fluorescence intensity is measured and presented in panel (G). Corresponding quantitation of THP1 cell adhesion is shown in panel (H). Levels of eNOS (I) and ET-1 (J) in the culture medium were measured. Bars represent 50 and 100 μm. EC: endothelial cell; Dox: doxorubicin. Statistical analysis was performed by one-way ANOVA. n = 5 per group. *P < 0.05, **P < 0.001, ***P < 0.001, and ****P < 0.0001.
Fig 2: Cytotoxic effect of doxorubicin on HUVECs. Representative fluorescent images of actin filaments (phalloidin, green fluorescence) showing morphology of endothelial cells stimulated by different concentrations of doxorubicin for 24 h at low (A) and high magnifications (B). Representative immunofluorescent images of ICAM1 (red fluorescence) of endothelial cells stimulated by different concentrations of doxorubicin for 24 h at low (C) and high magnifications (D). Representative immunofluorescent images of THP1 cell (orange fluorescence) and endothelial cell adhesion (green fluorescence) stimulated by different concentrations of doxorubicin at high magnifications (E). Quantitation of cell numbers per view is measured and presented in panel (F). Quantitation of mean fluorescence intensity is measured and presented in panel (G). Quantitation of THP1 cell adhesion is shown in panel (H). Levels of eNOS (I) and ET-1 (J) in the culture medium were measured. Bars represent 50 and 100 μm. n = 5 per group. EC: endothelial cell; Dox: doxorubicin. Statistical analysis was performed by one-way ANOVA. n = 5 per group. *P < 0.05, ***P < 0.001, and ****P < 0.0001.
Fig 3: ET-1 levels in SLE patients from validation cohort. (A) Comparison of serum ET-1 levels in SLE patients (N = 102) and diseases controls (N = 252, including 90 RA, 95 OA, 55 SS, 38 AS, 17 SSc) by ELISA. (B–F) Receiver operating characteristic curve analysis was used to assess potential of serum ET-1 in differentiating SLE from RA, OA, SS, AS, and SSc. (G) Analysis of difference in serum ET-1 between SLE and non-SLE patients. (H) Receiver operating characteristic curve analysis of serum ET-1 between SLE and non-SLE patients.
Fig 4: Linkage disequilibrium (LD) analysis for ten SNPs in ET-1 gene. The color and numerical value (D’) of each box represent the Te intensity of LD. Red and pink indicate significant linkage, light blue and white indicate no linkage. The value of D’ varies from 0 to 1, by which value of 1 represents the maximum link. Block 1 consists of rs6458155 and rs4145451. Block 2 consists of rs2071942, rs2071943 and rs5370.
Fig 5: Comparison of ET-1 levels between SLE patients and healthy controls in the training cohort. (A) Serum ET-1 levels in 53 SLE patients and 80 healthy individuals were examined by ELISA. Each symbol stands for an independent sample. (B–D) ET-1 levels in SLE patients distributed according to alopecia, proteinuria and anti-Sm. (E) Difference of serum levels of ET-1 in SLE patients with less active disease and active disease. (F–G) Relationship between ET-1 levels and SLEDAI, ESR levels. (H) Receiver operating characteristic curve analysis of serum ET-1 as a biomarker for SLE.
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