Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

Article Title: Resistin Enhances Monocyte Chemoattractant Protein-1 Production in Human Synovial Fibroblasts and Facilitates Monocyte Migration.

doi: 10.33594/000000029

Figure Lengend Snippet: Fig. 5. Resistin promotes MCP-1-mediated monocyte migration by inhibiting miR-33a and miR-33b. (A&B) OASFs were incubated with resistin for 24 h and miRNA expression was examined by qPCR. (C) OASFs were transfected with the miR-33a and miR-33b mimics then incubated with resistin for 24 h; MCP-1 expression was measured by qPCR. (D) CM was applied to THP-1 cells and analyzed for migration activity. Results are expressed as the mean ± SEM. *p<0.05 as compared with the control group; #p<0.05 as compared with the resistin-treated group.

Article Snippet: KG Chen et al.: Resistin Enhances MCP-1-Mediated Monocyte Migration Materials and Methods Materials Recombinant human resistin was purchased from R&D Systems (Minneapolis, MN, USA).

Techniques: Migration, Incubation, Expressing, Transfection, Activity Assay, Control

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: Resistin induces HCT-116 and SW-48 cell adhesion to HUVECs. HCT-116 and SW-48 cells were maintained as controls or stimulated with resistin and then stained with a crystal violet solution. The adhesion of HCT-116 and SW-48 cells to HUVECs was assessed. HCT-116 and SW-48 cells incubated with resistin (50 ng/mL) plus resistin-neutralizing antibodies (Ab) exhibited no increase in HUVEC adhesion. Data represent the mean ± standard error of the mean (SEM) from four independent experiments. * p < 0.05 vs. control cells; # p < 0.05 vs. cells treated with resistin only.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Staining, Incubation, Control

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: Resistin increases the expressions of ICAM-1 and VCAM-1 in HCT-116 cells. HCT-116 cells were maintained as control or stimulated with resistin. ICAM-1 and VCAM-1 mRNA ( A , B ) and protein ( C , D ) expression was analyzed. Data in ( A , B ) represent the mean ± SEM from three independent experiments. The results in ( C , D ) are representative of three independent experiments with similar results. * p < 0.05 vs. control cells.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Control, Expressing

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: Blocking ICAM-1 and VCAM-1 in HCT-116 cells inhibits their adhesion to HUVECs. HCT-116 cells were pretreated with specific neutralizing antibodies ( A ) or siRNAs ( B ) for control (IgG/si-CL), ICAM-1, VCAM-1, or both and then were maintained as control or stimulated with resistin. HCT-116 cell adhesion was determined. Data represent the mean ± SEM from four independent experiments. * p < 0.05 vs. control cells (CL); # p < 0.05 vs. cells pretreated with IgG or si-CL and then treated with resistin only; ** p < 0.05 vs. cells pretreated with ICAM-1 or VCAM-1 neutralizing antibody and then treated with resistin.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Blocking Assay, Control

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: Resistin-initiated HCT-116 adhesion to HUVECs is mediated by NF-κB activation. ( A ) and ( C ) HCT-116 cells were maintained as control or stimulated with resistin for 1, 2, and 4 h and then NF-κB activation ( A ) and p65 phosphorylation ( C ) were determined by ELISA kit and Western blot, respectively; ( B , D , E ) HCT-116 cells were pretreated with ( B , D ) DMSO or NF-κB inhibitors (PDTC or SN50) and ( E ) control or p65 specific siRNA and then stimulated with resistin. HCT-116 cell adhesion and ICAM-1/VCAM-1 mRNA expression were analyzed. Data represent the mean ± SEM from three independent experiments. * p < 0.05 vs. control cells; # p < 0.05 vs. DMSO or si-CL cells with resistin treatment; § p < 0.05 vs. PDTC, SN50, or si-p65 cells without resistin treatment.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Activation Assay, Control, Phospho-proteomics, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: FA inhibits resistin-initiated HCT-116 cell adhesion to HUVECs. ( A ) HCT-116 cells were pretreated with FA at 0, 1, 5 and 10 μg/mL and then were maintained as control or stimulated with resistin; ( B ) HCT-116 cells were pretreated with FA at 0 or 10 μg/mL and then were maintained as control or stimulated with resistin at 10, 25 and 50 ng/mL. HCT-116 cell adhesion was determined. Data represent the mean ± SEM from three independent experiments. * p < 0.05 vs. control cells; # p < 0.05 vs. cells treated with resistin only.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Control

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: FA inhibits resistin-induced ICAM-1 and VCAM-1 expression in HCT-116 cells. HCT-116 cells were pretreated with FA at 0, 1, 5 and 10 μg/mL and then were maintained as control or stimulated with resistin. ICAM-1 and VCAM-1 mRNA ( A , B ) and protein ( C , D ) expression was determined. Data in ( A , B ) represent the mean ± SEM from three independent experiments. The results in ( C , D ) are representative of three independent experiments with similar results. * p < 0.05 vs. control cells; # p < 0.05 vs. cells treated with resistin only.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Expressing, Control

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: FA inhibits the resistin effect on HCT-116 cell adhesion to HUVECs by down-regulating NF-κB activity. HCT-116 cells were pretreated with FA at 0, 1, 5 and 10 μg/mL and then were maintained as control or stimulated with resistin. The activation of NF-κB was determined. Data represent the mean ± SEM from three independent experiments. * p < 0.05 vs. control cells; # p < 0.05 vs. cells treated with resistin only.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Activity Assay, Control, Activation Assay

Journal: The American journal of pathology

Article Title: Interaction between Esophageal Squamous Cell Carcinoma and Adipose Tissue in Vitro.

doi: 10.1016/j.ajpath.2016.01.003

Figure Lengend Snippet: Figure 9 Effects of adipokines on growth (A) and apoptosis (B) of cancer cells alone and of IGF-1 and IGF-1R inhibitor (PPP) on structure (DeI) and apoptosis (C) of cancer cells alone. Immunohistochemistry with the growth marker Ki-67 (A) and the apoptosis marker cleaved caspase-3 (B and C) and morphologic analysis (DeI) are performed in cancer cells treated with IGF-1, leptin, adiponectin, resistin, or PPP, as described in Materials and Methods. IGF-1 significantly promotes Ki-67 expression in both EC-GI-10 and TE-9 cells (A), whereas leptin, adiponectin, and resistin do not affect that in both cell types. IGF-1 significantly inhibits cleaved caspase-3 expression in both EC-GI-10 and TE-9 cells (B), whereas leptin, adiponectin, and resistin do not affect that in both cell types. IGF-1R inhibitor (PPP) significantly promotes cleaved caspase-3 expression in both EC-GI-10 and TE-9 cells (C). Both EC-GI-10 and TE-9 cells treated with IGF-1 (E and H) replicate the ATF-induced structure, in comparison with cell types not treated with IGF-1 (D and G). Interestingly, IGF-1R inhibitor (PPP) drastically inhibits the stratification of EC-GI-10 and TE-9 cells (F and I), showing morphologic apoptosis of them. Data are expressed as means SD. **P < 0.01. Scale bar Z 50 mm. ATF, adipose tissue fragment; IGF, insulin-like growth factor; PPP, picropodophyllin.

Article Snippet: To examine the effects of leptin, adiponectin, resistin, IGF-1, and IGF-1R inhibitor on the structure, proliferation, and apoptosis of ESCC cells, recombinant rat leptin (1 ng/mL; R&D Systems, Inc.), recombinant rat adiponectin (1 mg/mL; Aviscera Bioscience, Inc., Santa Clara, CA), resistin (30 ng/mL; OriGene EU, Herford, Germany), recombinant animal-free human IGF-1 (10 nmol/L; Merck Millipore Corp.), and picropodophyllin (PPP; 1 mmol/L; Merck Millipore Corp.) were added to the culture medium for 3 days.

Techniques: Immunohistochemistry, Marker, Expressing, Comparison