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: Journal of biomedical science

Article Title: Neutrophil-derived reactive agents induce a transient SpeB negative phenotype in Streptococcus pyogenes.

doi: 10.1186/s12929-023-00947-x

Figure Lengend Snippet: Fig. 1 Reversible loss of SpeB is associated with tissue pathology and inflammation. A Distribution of SpeB+ and SpeB− GAS clones directly isolated from NSTI patient tissue biopsies (n = 23). B Percentage of SpeB+ and SpeB− GAS clones after the passage in THY media (p1, passage 1; p2, passage 2). Representative analysis of 2006 GAS patient isolate is shown. C–G Correlation analysis of bacterial load (left panel; n = 81 biopsies) or percentage of SpeB− clones (right panel; n = 23 biopsies) with the presence of HMGB1 (C), IL-8 (D), infiltrating neutrophils (E), and resistin (F) in patient biopsies. Correlation was determined using Spearman test. Semiquantitative acquired computerized image analyses (ACIA) of immuno-histochemical staining were performed as described in the methods section. The cell area was defined by the hematoxylin counterstaining, and the results are presented as percent positively stained area × mean intensity of positive staining

Article Snippet: The following antibodies were used for immunohistochemistry: anti-human HMGB1 (clone EPR3507; Abcam), anti-human IL-8 (clone NAP-1; Invitrogen), anti-human resistin (clone 184,305; R&D systems), and anti-human neutrophilelastase (clone NP57; DAKO).

Techniques: Clone Assay, Isolation, Staining

Journal: Cell death & disease

Article Title: Deletion of Mettl3 in mesenchymal stem cells promotes acute myeloid leukemia resistance to chemotherapy.

doi: 10.1038/s41419-023-06325-7

Figure Lengend Snippet: Fig. 1 Deletion of Mettl3 in MSCs induces high marrow adiposity in mice. A Western blot analysis of METTL3 in BMMSCs isolated from mice. B Detections of m6A levels in total RNA in BMMSCs from mice using EpiQuik m6A RNA Methylation Quantification Kits. C Representative images of H&E staining and FABP4 immunohistochemical staining of the distal femora from mice. Scale Bars: 100 μm. D Quantification of adipocyte number and area per tissue area in the distal marrow (n = 8). E ELISA examined the contents of supernatant adipokines in bone marrow rinses of mice (n = 6). F Representative images and quantitative analyses of Alizarin Red Solution (ARS) staining of BMMSCs isolated from mice. Scale Bars: 200 μm. G Representative images and quantitative analyses of ORO staining of BMMSCs isolated from mice. Scale Bars: 200 μm. The data are presented as mean ± SD. The two-tailed unpaired Student’s t test was used to compare two groups and one-way ANOVA with Dunnett’s multiple comparisons test was used for data with more than two groups. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns not significant.

Article Snippet: In the supernatant, based on the Cell Death and Disease (2023) 14:796 manufacturer’s directions, the levels of adipokines, like resistin, leptin, and growth hormone, were quantified employing the kits of Mouse Resistin ELISA (Cat# CSB-E06886m, CUSABIO, Wuhan, Hubei, China), Mouse Leptin ELISA (Cat# CSB-E04650m, CUSABIO), and Mouse Growth Hormone ELISA (Cat# CSB-E07343m, CUSABIO), respectively.

Techniques: Western Blot, Isolation, Methylation, Staining, Immunohistochemical staining, Enzyme-linked Immunosorbent Assay, Two Tailed Test

Journal: Cell death & disease

Article Title: Deletion of Mettl3 in mesenchymal stem cells promotes acute myeloid leukemia resistance to chemotherapy.

doi: 10.1038/s41419-023-06325-7

Figure Lengend Snippet: Fig. 4 METTL3 deletion reduces AML chemosensitivity by inducing adipogenic differentiation of OP9 cells. A Representative images and quantification of ORO staining in Mettl3 overexpression cells after 14 days of adipogenic induction. Scale bar, 100 µm. B qPCR analysis of the expression of adipogenic marker genes, Adipoq, Cebpa, Lpl, Plin1, CD36, and Pparγ in Mettl3 overexpression cells under adipogenic conditions. C ORO staining of Mettl3 knockdown cells following adipogenic induction. Scale bar, 100 µm. Absorbance at OD500 was determined for ORO staining in isopropanol at room temperature. D qPCR analysis of adipogenic lineage–associated gene expression after induction of differentiation in Mettl3 knockdown cells. E ELISA detection of adipokine concentration in the culture medium before induction of differentiation and on day 14 of Mettl3 overexpression cells. F ELISA detection of adipokine concentration in the culture medium before induction of differentiation and on day 14 of Mettl3 knockdown cells. G After adipogenic differentiation of Mettl3 overexpression cells, AML cells were co-cultured with them for 24 h to test their chemoresistance to Ara-C and DNR. H After adipogenic differentiation of Mettl3 knockdown cells, AML cells were co-cultured with them for 24 h to test their chemoresistance to Ara-C and DNR. Blank, blank control; OE-NC, negative control of overexpression; Mettl3-OE, overexpression of mouse Mettl3; sh-NC, negative control of knockdown; shMettl3-1 and shMettl3-2, independent shRNAs targeting mouse Mettl3. The data are presented as mean ± SD. The two-tailed unpaired Student’s t test was used to compare two groups and one-way ANOVA with Dunnett’s multiple comparisons test was performed for multiple groups. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns not significant.

Article Snippet: In the supernatant, based on the Cell Death and Disease (2023) 14:796 manufacturer’s directions, the levels of adipokines, like resistin, leptin, and growth hormone, were quantified employing the kits of Mouse Resistin ELISA (Cat# CSB-E06886m, CUSABIO, Wuhan, Hubei, China), Mouse Leptin ELISA (Cat# CSB-E04650m, CUSABIO), and Mouse Growth Hormone ELISA (Cat# CSB-E07343m, CUSABIO), respectively.

Techniques: Staining, Over Expression, Expressing, Marker, Knockdown, Gene Expression, Enzyme-linked Immunosorbent Assay, Concentration Assay, Cell Culture, Control, Negative Control, Two Tailed Test

Journal: Cell death & disease

Article Title: Deletion of Mettl3 in mesenchymal stem cells promotes acute myeloid leukemia resistance to chemotherapy.

doi: 10.1038/s41419-023-06325-7

Figure Lengend Snippet: Fig. 6 AKT inhibitor MK2206 mediates the adipogenesis level of OP9 cells. A Western blot analysis of AKT and p-AKT1 (Ser473) in OP9 cells treated with MK2206, an AKT inhibitor. B ORO staining of DMSO and MK2206 treated cells after adipo-induced for 14 days. Scale bar, 100 μm. C ELISA detected the concentration of adipokines in the culture medium before induction of differentiation and on day 14 under treatment with MK2206. D After being treated with MK2206 for 18 h and adipo-induced for 14 days, co-culturing with AML cells for 24 h was performed to test the chemoresistance of AML cells to Ara-C and DNR. The data are presented as mean ± SD. The two-tailed unpaired Student’s t test was used to compare two groups and one-way ANOVA with Dunnett’s multiple comparisons test was performed for multiple groups. *P < 0.05, **P < 0.01, ***P < 0.001, ns not significant.

Article Snippet: In the supernatant, based on the Cell Death and Disease (2023) 14:796 manufacturer’s directions, the levels of adipokines, like resistin, leptin, and growth hormone, were quantified employing the kits of Mouse Resistin ELISA (Cat# CSB-E06886m, CUSABIO, Wuhan, Hubei, China), Mouse Leptin ELISA (Cat# CSB-E04650m, CUSABIO), and Mouse Growth Hormone ELISA (Cat# CSB-E07343m, CUSABIO), respectively.

Techniques: Western Blot, Staining, Enzyme-linked Immunosorbent Assay, Concentration Assay, Two Tailed Test

Journal: The Journal of Clinical Hypertension

Article Title: Masked Hypertension and Atherogenesis: The Impact on Adiponectin and Resistin Plasma Levels

doi: 10.1111/j.1751-7176.2008.00070.x

Figure Lengend Snippet: Resistin and Adiponectin Plasma Levels of the Study Groups

Article Snippet: The adiponectin plasma levels (RD195023100; Human Adiponectin ELISA Bio Vendor Laboratory Medicine Inc, Brno, Czech Republic) and the resistin plasma levels (RD191016100; Human Resistin ELISA Bio Vendor Laboratory Medicine Inc.) were measured by immunoassay .

Techniques: Clinical Proteomics

Journal: Physiological Reports

Article Title: Estrogen receptor α activation modulates the gut microbiome and type 2 diabetes risk factors

doi: 10.14814/phy2.15344

Figure Lengend Snippet: Serum hormone changes with Ex, E 2 , propylpyrazoletriyl, and diarylpropionitrile (DPN) treatment. At the end of the 10 week study, blood was collected to measure the serum adiponectin (a), resistin (b) ghrelin (c), and leptin (d) levels via an ELISA. * p < 0.05 vs. control and DPN, ** p < 0.05 vs. control and Ex, *** p < 0.05 vs. control.

Article Snippet: The serum adiponectin (22‐ADPRT‐E01, ALPCO), leptin (EZRL‐83K, Millipore), ghrelin (EZRGRT‐91K, Millipore), and resistin (32–5179; ALPCO) levels were measured via an ELISA according to the manufacturer’s instructions.

Techniques: Enzyme-linked Immunosorbent Assay, Control

Journal: Osteoarthritis and cartilage

Article Title: Resistin is elevated following traumatic joint injury and causes matrix degradation and release of inflammatory cytokines from articular cartilage in vitro.

doi: 10.1016/j.joca.2008.08.007

Figure Lengend Snippet: Fig. 2. IHC staining of synovium (A, B) and cartilage (C, D) tissues from normal (A, C) and OA (B, D) patients with an anti-resistin antibody. The arrows indicate examples of the cells positively stained with anti-resistin antibody. Magnification is 40. The images are representative of sections taken from three patients.

Article Snippet: ANTIBODY IN JOINT TISSUES Fixed, paraffin embedded synovial and cartilage tissues from three healthy and three OA patient donors were analyzed by IHC with an anti-resistin antibody (R&D Systems, Minneapolis, MN).

Techniques: Immunohistochemistry, Staining