Journal: Journal of Advanced Research

Article Title: S100B induces angiogenesis via the clathrin/FOXO1/β-catenin signaling pathway and contributes to Bevacizumab resistance in epithelial ovarian cancer

doi: 10.1016/j.jare.2025.05.060

Figure Lengend Snippet: Flowchart of the study. First, BEV-sensitive and BEV-resistant ovarian cancer mouse models were constructed, and RNA sequencing was performed on tumor tissue. Then, a BEV-related prognostic signature was established using machine learning, and S100B was identified as the most important molecule regulating BEV sensitivity in ovarian cancer. Its function and mechanism were analyzed in vitro. Finally, BEV efficacy when combined with an S100B inhibitor was verified in vivo. BEV: Bevacizumab; DEGs: Differentially expressed genes.

Article Snippet: S100B and VEGFA levels in the supernatant were measured using S100B (Elabscience, E-EL-H1297) and VEGFA (Elabscience, E-EL-H0111) ELISA kits.

Techniques: Construct, RNA Sequencing, In Vitro, In Vivo

Journal: Journal of Advanced Research

Article Title: S100B induces angiogenesis via the clathrin/FOXO1/β-catenin signaling pathway and contributes to Bevacizumab resistance in epithelial ovarian cancer

doi: 10.1016/j.jare.2025.05.060

Figure Lengend Snippet: Screening S100B as the main molecule regulating the sensitivity of ovarian cancer to BEV. (A) Kaplan–Meier survival analysis of OS (left) and PFS (right) of patients with high S100B expression treated with chemotherapy with or without BEV (from the GSE140082 dataset). (B) Kaplan–Meier survival analysis of OS (left) and PFS (right) of patients with low S100B expression treated with chemotherapy with or without BEV (from the GSE140082 dataset). (C) Western blot analysis of S100B protein expression in tumor tissue from BEV-sensitive and BEV-resistant mice. (D) Western blot analysis of S100B protein levels in mouse tumor tissue. (E) Immunohistochemical staining of S100B protein in BEV-sensitive and BEV-resistant mice. (F) Statistical histochemical staining of S100B protein in mouse tumor tissue. BEV:Bevacizumab; **: P < 0.01.

Article Snippet: S100B and VEGFA levels in the supernatant were measured using S100B (Elabscience, E-EL-H1297) and VEGFA (Elabscience, E-EL-H0111) ELISA kits.

Techniques: Expressing, Western Blot, Immunohistochemical staining, Staining

Journal: Journal of Advanced Research

Article Title: S100B induces angiogenesis via the clathrin/FOXO1/β-catenin signaling pathway and contributes to Bevacizumab resistance in epithelial ovarian cancer

doi: 10.1016/j.jare.2025.05.060

Figure Lengend Snippet: Co-culture of S100B overexpressing ovarian cancer cells promotes HUEVC angiogenesis and migration. (A) Representative Western blot images and their densitometric quantification showing comparative S100B protein expression profiles among the three ovarian cancer cell lines (A2780, HEY, and OVCAR3) (B) Western blot analysis and statistical analysis of OVCAR3 and HEY cells overexpressing S100B. RT-qPCR analysis of alternative angiogenic factor mRNA expression levels in (C) OVCAR3 and (D) HEY ovarian cancer cell lines following S100B overexpression. (E) The level of S100B in the supernatant of OVCAR3 and HEY cells overexpressing S100B significantly increased, as determined by ELISA. (F) There was no significant change in VEGFA levels in the supernatant of OVCAR3 and HEY cells overexpressing S100B. (G, H) HUVEC tube formation significantly increased after co-culture with ovarian cancer cell lines overexpressing S100B, with or without exogenous BEV. (I, J) Co-culture with ovarian cancer cells overexpressing S100B significantly promoted HUVEC sprouting with or without exogenous BEV. (K, L) Co-culture of ovarian cancer cells overexpressing S100B significantly promoted migration of HUVECs in a Transwell system with or without exogenous BEV. (M, N) Co-culture of ovarian cancer cell lines overexpressing S100B significantly promoted healing of HUVECs with or without exogenous BEV in a scratch assay. BEV: Bevacizumab; NC: negative control; OE: overexpression; *: P < 0.05; **: P < 0.01; ***: P < 0.001; ****: P < 0.0001. Scale: All panels are 50 μm.

Article Snippet: S100B and VEGFA levels in the supernatant were measured using S100B (Elabscience, E-EL-H1297) and VEGFA (Elabscience, E-EL-H0111) ELISA kits.

Techniques: Co-Culture Assay, Migration, Western Blot, Expressing, Quantitative RT-PCR, Over Expression, Enzyme-linked Immunosorbent Assay, Wound Healing Assay, Negative Control

Journal: Journal of Advanced Research

Article Title: S100B induces angiogenesis via the clathrin/FOXO1/β-catenin signaling pathway and contributes to Bevacizumab resistance in epithelial ovarian cancer

doi: 10.1016/j.jare.2025.05.060

Figure Lengend Snippet: Exogenous recombinant S100B protein promoted vascular formation and migration of HUEVCs. Different concentrations of recombinant S100B protein, with or without BEV, promoted (A, B) angiogenesis in a tube formation assay, (C, D) sprouting in a fibrin bead sprouting assay, (E, F) migration in a Transwell assay, and (G, H) healing of endothelial cells in a wound healing assay. (I) Tip cell marker expression in HUVECs significantly increased by rt-qPCR detection after treatment with recombinant S100B protein. BEV: Bevacizumab; *: P < 0.05; **: P < 0.01; ***: P < 0.001; ****: P < 0.0001. Scale: All panels are 50 μm.

Article Snippet: S100B and VEGFA levels in the supernatant were measured using S100B (Elabscience, E-EL-H1297) and VEGFA (Elabscience, E-EL-H0111) ELISA kits.

Techniques: Recombinant, Migration, Tube Formation Assay, Transwell Assay, Wound Healing Assay, Marker, Expressing, Quantitative RT-PCR

Journal: Journal of Advanced Research

Article Title: S100B induces angiogenesis via the clathrin/FOXO1/β-catenin signaling pathway and contributes to Bevacizumab resistance in epithelial ovarian cancer

doi: 10.1016/j.jare.2025.05.060

Figure Lengend Snippet: S100B enters endothelial cells through clathrin-dependent endocytosis to promote angiogenesis and migration. (A) Western blot detection showed that there was no significant change in RAGE receptor expression in endothelial cells after exogenous S100B treatment. (B) Western blot detection showed that protein levels of S100B in endothelial cells significantly increased after co-culture with ovarian cancer cells overexpressing S100B. (C) S100B total protein and nuclear protein in endothelial cells significantly increased after treatment with exogenous S100B, as determined by western blot analysis. (D) Western blot analysis of protein levels of S100B in endothelial cells after pretreatment with the clathrin-mediated endocytosis inhibitor Pitstop-2 or caveolae/caveolin-1-mediated endocytosis inhibitor nystatin. Changes in the (F, G) tubular phenotype, (H, I) sprouting phenotype, (J, K) migration phenotype (Transwell assay), and (L–M) wound healing phenotype (scratch migration assay) of endothelial cells after treatment with the RAGE receptor inhibitor FPS-ZM1, the clathrin-mediated endocytosis inhibitor Pitstop-2, and the caveolae/caveolin-mediated endocytosis inhibitor nystatin. BEV: Bevacizumab; *: P < 0.05; **: P < 0.01; ***: P < 0.001; ****: P < 0.0001. Scale: All panels are 50 μm.

Article Snippet: S100B and VEGFA levels in the supernatant were measured using S100B (Elabscience, E-EL-H1297) and VEGFA (Elabscience, E-EL-H0111) ELISA kits.

Techniques: Migration, Western Blot, Expressing, Co-Culture Assay, Transwell Assay

Journal: Journal of Advanced Research

Article Title: S100B induces angiogenesis via the clathrin/FOXO1/β-catenin signaling pathway and contributes to Bevacizumab resistance in epithelial ovarian cancer

doi: 10.1016/j.jare.2025.05.060

Figure Lengend Snippet: S100B promotes tube formation and migration of endothelial cells through the FOXO1/β-catenin signaling pathway. (A) DIA proteomics thermogram of differentially expressed proteins in HUVECs with or without exogenous S100B. (B) Function and pathway enrichment analysis by Metascape database of differentially expressed proteins. (C–E) Western blot analysis showed that levels of S100B in ovarian cancer tissue of BEV-resistant mice significantly increased, while FOXO1 levels decreased. (F) Histogram of an RT-qPCR analysis of downstream transcriptional target genes of β-catenin. (G–J) Western blot analysis showed that FOXO1 total protein and nuclear protein levels in endothelial cells significantly decreased after treatment with exogenous S100B, while levels of β-catenin and MMP7 significantly increased. (K–M) Western blot analysis of FOXO1 and β-catenin levels in S100B-treated endothelial cells overexpressing FOXO1 compared with the control group. Endothelial cells transfected with a control virus or FOXO1 -overexpressing lentivirus and treated with S100B were evaluated for their (N) tubular phenotype by tube formation assay, (O) sprouting phenotype by fibrin bead sprouting assay, and (P) migration phenotype by Tranwell assay. (Q) Schematic diagram of the mechanism of exogenous S100B on endothelial cell angiogenesis. *: P < 0.05; **: P < 0.01;^: P < 0.05 vs. S100B−/oeFOXO1−; #: P < 0.05 vs. S100B−/oeFOXO1+; &: P < 0.05 vs. S100B+/oeFOXO1 − . Scale: All panels are 50 μm.

Article Snippet: S100B and VEGFA levels in the supernatant were measured using S100B (Elabscience, E-EL-H1297) and VEGFA (Elabscience, E-EL-H0111) ELISA kits.

Techniques: Migration, Western Blot, Quantitative RT-PCR, Control, Transfection, Virus, Tube Formation Assay

Journal: Journal of Advanced Research

Article Title: S100B induces angiogenesis via the clathrin/FOXO1/β-catenin signaling pathway and contributes to Bevacizumab resistance in epithelial ovarian cancer

doi: 10.1016/j.jare.2025.05.060

Figure Lengend Snippet: The S100B inhibitor pentamidine in combination with BEV improves the ovarian cancer response compared to BEV alone. (A) Flowchart of the in vivo experiment. Two weeks after intraperitoneal inoculation of ovarian cancer cells, drug treatment was administered. The mice were randomly divided into a normal saline treatment control group, BEV treatment group, pentamidine treatment group, and BEV with pentamidine treatment group. (B) Line chart of the tumor fluorescence intensity of the four groups of mice. (C) Tumor fluorescence imaging of mice after tumor formation (week 2), after killing the control group and pentamidine treatment group (week 4–6), after killing the BEV treatment group (week 8–9), and after killing the BEV with pentamidine treatment group (week 13–14). (D) Kaplan–Meier survival curves of the four groups of mice. (E) CD31 immunohistochemical staining and (F) MVD statistics of tumor tissue from the four groups of mice. (E) S100B immunohistochemical staining and S100B (G) staining intensity of tumor tissue from the four groups of mice. BEV: Bevacizumab; MVD: Micro-vessel density; *: P < 0.05; **: P < 0.01;^: P < 0.05 vs. NC; #: P < 0.05 vs. pentamidine; &: P < 0.05 vs. BEV.

Article Snippet: S100B and VEGFA levels in the supernatant were measured using S100B (Elabscience, E-EL-H1297) and VEGFA (Elabscience, E-EL-H0111) ELISA kits.

Techniques: In Vivo, Saline, Control, Fluorescence, Imaging, Immunohistochemical staining, Staining

Journal: Journal of Clinical Biochemistry and Nutrition

Article Title: Identification and validation of lactylation-related diagnostic biomarkers for type 2 diabetes by WGCNA

doi: 10.3164/jcbn.25-245

Figure Lengend Snippet: Identification of signature genes in T2D and evaluation of their diagnostic value. (A) Identification of signature genes through LASSO analysis. (B) Identification of signature genes using SVM-RFE analysis. (C) Identification of signature genes by RF analysis, with the figure showing the feature importance ranking. (D) Venn diagram illustrating the overlap of signature genes identified by the three machine learning algorithms. (E) Comparison of expression levels of consensus genes (identified by all three algorithms) between control and T2D groups. (F) ROC curves of diagnostic genes in the training set. (G) ROC curves of diagnostic genes in the validation set. (H) The mRNA levels of IKZF1, S100A4, and VIM in the cells were detected by qRT-PCR. (I) The protein levels of IKZF1, S100A4, and VIM in the cells were detected by WB. *** p <0.001, **** p <0.0001.

Article Snippet: To investigate the significance of IKZF1, S100A4, and VIM in T2D, we treated MIN6 cells with or without 200 μM palmitic acid (MCE) and 25 mM glucose (MCE) to establish an in vitro diabetic model, and set up groups: Con and Model. qRT-PCR and WB analysis showed that compared with the Con group, the mRNA and protein levels of IKZF1, S100A4, and VIM were significantly upregulated in the Model group ( H and I).

Techniques: Diagnostic Assay, Comparison, Expressing, Control, Biomarker Discovery, Quantitative RT-PCR

Journal: Journal of Clinical Biochemistry and Nutrition

Article Title: Identification and validation of lactylation-related diagnostic biomarkers for type 2 diabetes by WGCNA

doi: 10.3164/jcbn.25-245

Figure Lengend Snippet: Functional pathway enrichment characteristics of diagnostic genes based on GSVA analysis. (A, B) GO (A) and KEGG (B) enrichment analyses of the diagnostic gene IKZF1. (C, D) GO (C) and KEGG (D) enrichment analyses of the diagnostic gene S100A4. (E, F) GO (E) and KEGG (F) enrichment analyses of the diagnostic gene VIM.

Article Snippet: To investigate the significance of IKZF1, S100A4, and VIM in T2D, we treated MIN6 cells with or without 200 μM palmitic acid (MCE) and 25 mM glucose (MCE) to establish an in vitro diabetic model, and set up groups: Con and Model. qRT-PCR and WB analysis showed that compared with the Con group, the mRNA and protein levels of IKZF1, S100A4, and VIM were significantly upregulated in the Model group ( H and I).

Techniques: Functional Assay, Diagnostic Assay

Journal: Journal of Clinical Biochemistry and Nutrition

Article Title: Identification and validation of lactylation-related diagnostic biomarkers for type 2 diabetes by WGCNA

doi: 10.3164/jcbn.25-245

Figure Lengend Snippet: Analysis of immune infiltration characteristics and correlation with diagnostic genes. (A) Boxplots comparing immune cell and functional infiltration between T2D and control groups using ssGSEA algorithm. (B) Correlation analysis between IKZF1 and infiltrating immune cells/functions in T2D. (C) Correlation analysis between S100A4 and infiltrating immune cells/functions in T2D. (D) Correlation analysis between VIM and infiltrating immune cells/functions in T2D. ns, not significant; p >0.05; * p <0.05, ** p <0.01, *** p <0.001.

Article Snippet: To investigate the significance of IKZF1, S100A4, and VIM in T2D, we treated MIN6 cells with or without 200 μM palmitic acid (MCE) and 25 mM glucose (MCE) to establish an in vitro diabetic model, and set up groups: Con and Model. qRT-PCR and WB analysis showed that compared with the Con group, the mRNA and protein levels of IKZF1, S100A4, and VIM were significantly upregulated in the Model group ( H and I).

Techniques: Diagnostic Assay, Functional Assay, Control

Journal: Journal of Clinical Biochemistry and Nutrition

Article Title: Identification and validation of lactylation-related diagnostic biomarkers for type 2 diabetes by WGCNA

doi: 10.3164/jcbn.25-245

Figure Lengend Snippet: Prediction analysis of miRNA and TFs regulatory networks. (A) PPI network of miRNAs with IKZF1, S100A4, and VIM. (B) PPI network of TFs with IKZF1, S100A4, and VIM. Red circles represent diagnostic genes. Blue squares represent miRNAs. Blue circles represent TFs.

Article Snippet: To investigate the significance of IKZF1, S100A4, and VIM in T2D, we treated MIN6 cells with or without 200 μM palmitic acid (MCE) and 25 mM glucose (MCE) to establish an in vitro diabetic model, and set up groups: Con and Model. qRT-PCR and WB analysis showed that compared with the Con group, the mRNA and protein levels of IKZF1, S100A4, and VIM were significantly upregulated in the Model group ( H and I).

Techniques: Diagnostic Assay

Journal: Journal of Clinical Biochemistry and Nutrition

Article Title: Identification and validation of lactylation-related diagnostic biomarkers for type 2 diabetes by WGCNA

doi: 10.3164/jcbn.25-245

Figure Lengend Snippet: Knocking down IKZF1, S100A4, and VIM can reduce their lactate levels and increase the viability of pancreatic β cells. (A) Transfection efficiency assessment using qRT-PCR. (B) Detection of the total protein lactate levels in each group by WB. (C) Measurement of the cell survival rate in each group using the CCK-8 assay. **** p <0.0001.

Article Snippet: To investigate the significance of IKZF1, S100A4, and VIM in T2D, we treated MIN6 cells with or without 200 μM palmitic acid (MCE) and 25 mM glucose (MCE) to establish an in vitro diabetic model, and set up groups: Con and Model. qRT-PCR and WB analysis showed that compared with the Con group, the mRNA and protein levels of IKZF1, S100A4, and VIM were significantly upregulated in the Model group ( H and I).

Techniques: Transfection, Quantitative RT-PCR, CCK-8 Assay

Journal: Scientific Reports

Article Title: S100A8 regulated by estrogen improves injured endometrial epithelium reconstruction by promoting tight junction formation and stromal cell transformation

doi: 10.1038/s41598-025-08530-0

Figure Lengend Snippet: Effects of estrogen treatment on S100A8 expression in endometrium and epithelium morphology. ( a ) S100A8 immunohistochemical staining before and after estrogen treatment (1d/7d); black arrows indicate S100A8-positive immune cells (S100A8-PICs).The blue arrow indicates the release of S100A8 from S100A8-PICs. Scale bar is 100 or 400 μm. ( b ) Rat endometrial hematoxylin–eosin staining before and after estrogen treatment (1d/7d); red arrows show disrupted cell junctions. Scale bar is 100 μm. ( c ) S100A8-PICs number in the endometrium (1/mm 2 ) before and 1 d/7d after estrogen treatment (n = 18, from six rats, the number was counted from three immunohistochemical images of each sample , mean ± SEM). ( d ) S100A8 expression in the epithelium before and 1 d/7d after estrogen treatment (n = 18, from six rats, the expression level was measured from three immunohistochemical images of each sample, mean ± SEM). * Results with P values < 0.05 were considered significant. ** Results with P values < 0.01 were considered very significant.

Article Snippet: The cultured cells were randomly divided into three groups according to the experimental design: the control, S100A8 (0.5 μg/mL, HY- P71275 ; MCE, Shanghai, China), and S100A8 + FPS-ZM 1 (5 μM, HY-19370; MCE, Shanghai, China) groups.

Techniques: Expressing, Immunohistochemical staining, Staining

Journal: Scientific Reports

Article Title: S100A8 regulated by estrogen improves injured endometrial epithelium reconstruction by promoting tight junction formation and stromal cell transformation

doi: 10.1038/s41598-025-08530-0

Figure Lengend Snippet: Effects of uterine cavity administration of S100A8 on the distribution of S100A8-PICs and endometrial morphology. ( a ) Distribution of S100A8-positive cells in the endometrium of four different groups with estrogen treatment (control, injury, P407, and S100A8 + P407 groups). Black arrows show S100A8-PICs. S100A8-PICs were distributed around the glands and blood vessels in the control group. S100A8-PICs in the site of injury or adhesion in the injury group and in the P407 group. S100A8-PICs reverse migrated to the glands or blood vessels in the S100A8 + P407 group. Scale bar is 100 μm or 1 mm. ( b ) Endometrial thickness in the four groups (n = 15, from 5 rats; 3 position was measured randomly in an image of each rat, mean ± SEM). ( c ) The number of endometrial glands in each group (n = 10, from 10 rats, glands were counted from a uterine horn cross-section image at 40 × of each rat, mean ± SEM). ( d ) The interior wall integrity of uterine cavity in each group (n = 10, from 10 rats, data was measured from a uterine horn cross-section image at 40 × of each rat, mean ± SEM). ( e ) The number of endometrial crypts in each group (n = 10, from 10 rats, crypts were counted from a uterine horn cross-section image at 40 × of each rat, mean ± SEM). * Results with P values < 0.05 were considered significant. ** Results with P values < 0.01 were considered very significant.

Article Snippet: The cultured cells were randomly divided into three groups according to the experimental design: the control, S100A8 (0.5 μg/mL, HY- P71275 ; MCE, Shanghai, China), and S100A8 + FPS-ZM 1 (5 μM, HY-19370; MCE, Shanghai, China) groups.

Techniques: Control

Journal: Scientific Reports

Article Title: S100A8 regulated by estrogen improves injured endometrial epithelium reconstruction by promoting tight junction formation and stromal cell transformation

doi: 10.1038/s41598-025-08530-0

Figure Lengend Snippet: Effects of S100A8 on the distribution of Ki-67-positive proliferating cells in the uteri and the proliferation of endometrial cells. ( a ) Ki-67-positive proliferating cells were distributed in the endometrium or uterine interior wall in all groups (control, injury, P407, and S100A8 + P407 groups). Scale bar is 100 or 400 μm. ( b ) Number of Ki-67-positive cells in the endometrium of each group (n = 20, from ten rats, the number was counted from two immunohistochemical images of each sample, mean ± SEM). ( c ) Number of Ki-67-positive cells in the uterine interior wall of each group (n = 20, from ten rats, the number was counted from two immunohistochemical images of each sample, mean ± SEM). ( d ) Effects of S100A8 and its receptor inhibitor (FPS-ZM1) on the proliferation of cultured endometrial cells in vitro (n = 5, mean ± SEM). Scale bar is 100 μm. * Results with P values < 0.05 were considered significant. ** Results with P values < 0.01 were considered very significant.

Article Snippet: The cultured cells were randomly divided into three groups according to the experimental design: the control, S100A8 (0.5 μg/mL, HY- P71275 ; MCE, Shanghai, China), and S100A8 + FPS-ZM 1 (5 μM, HY-19370; MCE, Shanghai, China) groups.

Techniques: Control, Immunohistochemical staining, Cell Culture, In Vitro

Journal: Scientific Reports

Article Title: S100A8 regulated by estrogen improves injured endometrial epithelium reconstruction by promoting tight junction formation and stromal cell transformation

doi: 10.1038/s41598-025-08530-0

Figure Lengend Snippet: Effects of S100A8 on tight junctions of endometrial epithelium or endometrial cells. ( a ) Immunohistochemical staining showing Claudin-1 distribution in the endometrium of different groups (control, injury, P407, and P407 + S100A8 groups); black arrows show Claudin-1 accumulated below the cell membrane of the lateral contact zone between adjacent cells and red arrows show cells expressing Claudin-1 in the stroma. Scale bar is 100 μm. ( b ) Claudin-1 expression in the endometrium of different groups (n = 10, mean ± SEM). ( c ) Western blot showing ZO-1 expression in endometrial cells of three different groups (control, S100A8, and S100A8 + FPS-ZM1 groups, n = 3, mean ± SEM). Actin was used as the loading control. The full-length bands can be found in supplementary Fig. 1. The bands of ZO-1 and actin cropped from different parts of the same gel. ( d ) Immunofluorescence showing the co-expression of Claudin-1 (red) and ZO-1 (green) in the endometrial cells of the three groups (n = 5, mean ± SEM). The nucleus is stained blue. The scale bar is 200 μm. * Results with P values < 0.05 were considered significant. ** Results with P values < 0.01 were considered very significant.

Article Snippet: The cultured cells were randomly divided into three groups according to the experimental design: the control, S100A8 (0.5 μg/mL, HY- P71275 ; MCE, Shanghai, China), and S100A8 + FPS-ZM 1 (5 μM, HY-19370; MCE, Shanghai, China) groups.

Techniques: Immunohistochemical staining, Staining, Control, Membrane, Expressing, Western Blot, Immunofluorescence

Journal: Scientific Reports

Article Title: S100A8 regulated by estrogen improves injured endometrial epithelium reconstruction by promoting tight junction formation and stromal cell transformation

doi: 10.1038/s41598-025-08530-0

Figure Lengend Snippet: Effects of S100A8 on endometrial “double-featured” cells. ( a ) Vimentin (red) and ZO-1 (green) immunofluorescent double staining of cultured endometrial cells. Scale bar is 200 μm. ( b ) Western blot showing CK-18 and vimentin expression in endometrial cells from each group (control, S100A8, and FPS-ZM1 groups; n = 3, mean ± SEM). The full-length bands can be found in supplementary Fig. 1. Actin was used as the loading control. As the target proteins have a similar molecular weight to that of the loading control, the bands of CK18/vimentin and actin were cropped from different gels. ( c ) Immunofluorescence showing vimentin expression in endometrial cells of each group (n = 5, mean ± SEM). Scale bar is 200 μm. * Results with P values < 0.05 were considered significant. ** Results with P values < 0.01 were considered very significant.

Article Snippet: The cultured cells were randomly divided into three groups according to the experimental design: the control, S100A8 (0.5 μg/mL, HY- P71275 ; MCE, Shanghai, China), and S100A8 + FPS-ZM 1 (5 μM, HY-19370; MCE, Shanghai, China) groups.

Techniques: Double Staining, Cell Culture, Western Blot, Expressing, Control, Molecular Weight, Immunofluorescence

Journal: Journal of neuroscience research

Article Title: Probing nano-organization of astroglia with multi-color super-resolution microscopy.

doi: 10.1002/jnr.24026

Figure Lengend Snippet: Fig. 3. Comparison of GFAP, glutamine synthetase and S100b expression in mixed cortical cultures. (A-T) Wide field and dSTORM images of astrocyte compartments in mixed cortical cultures, with the same notation and labeling as in Fig. 2. Scale bars: A-H and K-R, 5 mm; I-J and S-T, 1 mm.

Article Snippet: The marker proteins we used included glutamine synthetase (abcam, Cat# ab64613, RRID: AB_1140869 or Merck Millipore, Cat# MAB302, RRID: AB_2110656) (Derouiche and Frotscher, 1991; Volterra et al., 2014b) and the calciumbinding protein S100b (Synaptic Systems, Cat# 287 003, RRID: AB_2620024).

Techniques: Comparison, Expressing, Labeling

Journal: Journal of neuroscience research

Article Title: Probing nano-organization of astroglia with multi-color super-resolution microscopy.

doi: 10.1002/jnr.24026

Figure Lengend Snippet: Fig. 6. Nanoscopy of glutamine synthetase and S100b in GFAP-expressing cells in brain tissue sec- tions. (A-T) Wide field and dSTORM images of astrocyte compartments in brain tissue sections. Notation and labeling are the same as in Fig. 2 and 3. Scale bars: A-H and K-R, 5 mm; I-J and S- T, 1 mm.

Article Snippet: The marker proteins we used included glutamine synthetase (abcam, Cat# ab64613, RRID: AB_1140869 or Merck Millipore, Cat# MAB302, RRID: AB_2110656) (Derouiche and Frotscher, 1991; Volterra et al., 2014b) and the calciumbinding protein S100b (Synaptic Systems, Cat# 287 003, RRID: AB_2620024).

Techniques: Expressing, Labeling