recombinant mouse s100β novus biologicals nbp2 53070 b b homodimerizer takara  (Novus Biologicals)

Journal: Cell reports

Article Title: Cofilactin rod formation mediates inflammation-induced neurite degeneration

doi: 10.1016/j.celrep.2024.113914

Figure Lengend Snippet: S100β induces neurite loss (A and B) Low- and high-magnification views of brain sections from Thy1-YFP mice harvested 3 days after S100β injection. Scale bar: 500 μm. In (A), the arrow shows the injection site, and the rectangle shows the area of higher-magnification views shown in (B). In (B), neuronal cell nuclei are identified by NeuN immunostaining (magenta). Scale bar: 10 μm. (C) Quantification of neuronal cell body density. (D and E) YFP neurite length and area, expressed relative to saline-injected controls. n = 4; *p < 0.05 and **p < 0.01 vs. saline controls by one-way ANOVA with Dunnett’s test. All data are shown as mean ± SEM.

Article Snippet: Stereotaxic intracortical injections of lipopolysaccharide (LPS; Millipore), recombinant mouse S100β (Novus Biologicals) or saline (vehicle) were performed under 1.5% isoflurane anesthesia.

Techniques: Injection, Immunostaining, Saline

Journal: Cell reports

Article Title: Cofilactin rod formation mediates inflammation-induced neurite degeneration

doi: 10.1016/j.celrep.2024.113914

Figure Lengend Snippet: S100β induces cofilactin rod (CAR) formation and neurite loss (A) Diagram shows the locations of intracortical injections and peri-injection region imaged. (B) CAR formation identified by immunostaining for cofilin-1 aggregates (red) in WT mice after saline or 50 ng S100β injections. Neurites are identified by neurofilament-H (NF-H; green). NF-H integrity is lost at sites of CAR formation. Scale bar: 10 μm. (C–E) CAR density expressed as percentage of total neurite area. (F) Neurite loss 1, 3, and 7 days after saline or 50 ng S100β injections as assessed by immunostaining for NF-H (green), with neuronal cell nuclei identified by NeuN (magenta). Scale bar: 10 μm. (G–I) NF-H+ neurite length per neuronal nucleus in the S100β-injected mice. n = 4; **p < 0.01 by Student’s t test. All data are shown as mean ± SEM.

Article Snippet: Stereotaxic intracortical injections of lipopolysaccharide (LPS; Millipore), recombinant mouse S100β (Novus Biologicals) or saline (vehicle) were performed under 1.5% isoflurane anesthesia.

Techniques: Injection, Immunostaining, Saline

Journal: Cell reports

Article Title: Cofilactin rod formation mediates inflammation-induced neurite degeneration

doi: 10.1016/j.celrep.2024.113914

Figure Lengend Snippet: CAR formation is attenuated in both cofilin-1 hemizygous and p47 phox -deficient mice (A) CAR formation after saline or 50 ng S100β injections in WT, COF −/+ , and p47 phox−/− mice identified by immunostaining for cofilin-1 aggregates (red). Neurites are identified by NF-H (green). Scale bar: 10 μm. (B–D) CAR density expressed as percentage of total neurite area. (E) Neurite loss after saline or 50 ng S100β injections as assessed by immunostaining for NF-H (green), with neuronal cell nuclei identified by NeuN (magenta). Scale bar: 20 μm. (F–H) Neurite length per neuronal nucleus in the S100β-injected mice relative to saline-injected mice of each genotype. n = 4; *p < 0.05 and **p < 0.01 vs. WT mice by one-way ANOVA with Dunnett’s test. All data are shown as mean ± SEM.

Article Snippet: Stereotaxic intracortical injections of lipopolysaccharide (LPS; Millipore), recombinant mouse S100β (Novus Biologicals) or saline (vehicle) were performed under 1.5% isoflurane anesthesia.

Techniques: Saline, Immunostaining, Injection

Journal: Cell reports

Article Title: Cofilactin rod formation mediates inflammation-induced neurite degeneration

doi: 10.1016/j.celrep.2024.113914

Figure Lengend Snippet: S100β-induced neurite loss and motor impairment are attenuated in cofilin-1 hemizygous and p47 phox -deficient mice (A) Schematic timeline of behavioral assessments. (B) Performance on the corner test assessed by quantifying the percentage of left turns. n = 6 for each genotype. *p < 0.05 and **p < 0.01 vs. WT by one-way ANOVA with Dunnett’s test. (C) Iba-1 immunostaining shows microglial/macrophage (M/M) activation 1 day after injection with 50 ng S100β. Insets show magnified views. Responses to S100β injections were similar in the three mouse genotypes. Scale bars: 10 μm. (D–F) Quantification of M/M responses to S100β. n = 4; *p < 0.05 and **p < 0.01 vs. WT mice by one-way ANOVA with Dunnett’s test. All data are shown as mean ± SEM.

Article Snippet: Stereotaxic intracortical injections of lipopolysaccharide (LPS; Millipore), recombinant mouse S100β (Novus Biologicals) or saline (vehicle) were performed under 1.5% isoflurane anesthesia.

Techniques: Immunostaining, Activation Assay, Injection

Journal: Cell reports

Article Title: Cofilactin rod formation mediates inflammation-induced neurite degeneration

doi: 10.1016/j.celrep.2024.113914

Figure Lengend Snippet: Neurite loss in neuron-glia co-cultures is attenuated by neuronal cofilin-1 hemizygosity and glial p47 phox deficiency (A) Photomicrographs of co-cultures immunostained for MAP-2 (green) and NeuN (blue). Scale bar: 20 μm. (B–D) Neurite length assessed at 4, 24, and 48 h of 50 ng/mL S100β incubation, expressed relative to control wells of the respective co-culture type. n = 4; *p < 0.05 and **p < 0.01 by one-way ANOVA with Dunnett’s test. (E) Mechanism proposed for inflammation-induced neurite degeneration. In response to pro-inflammatory stimuli, brain microglia and infiltrating macrophages upregulate superoxide production by NADPH oxidase. Resulting oxidative stress in nearby neurites leads to formation of CARs. Persistence of the CARs causes neurite degeneration, which can occur in the absence of parental neuron death. This process is attenuated in p47 phox−/− mice, which cannot form an active NADPH oxidase-2 complex, and in cofilin hemizygous ( COF −/+ ) mice, which have reduced propensity to form CARs. All data are shown as mean ± SEM.

Article Snippet: Stereotaxic intracortical injections of lipopolysaccharide (LPS; Millipore), recombinant mouse S100β (Novus Biologicals) or saline (vehicle) were performed under 1.5% isoflurane anesthesia.

Techniques: Incubation, Control, Co-Culture Assay

Journal: Cell reports

Article Title: Cofilactin rod formation mediates inflammation-induced neurite degeneration

doi: 10.1016/j.celrep.2024.113914

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Stereotaxic intracortical injections of lipopolysaccharide (LPS; Millipore), recombinant mouse S100β (Novus Biologicals) or saline (vehicle) were performed under 1.5% isoflurane anesthesia.

Techniques: Affinity Purification, Recombinant, Membrane, Software

Journal: Molecular biomedicine

Article Title: Enteric glial cells aggravate the intestinal epithelial barrier damage by secreting S100β under high-altitude conditions.

doi: 10.1186/s43556-023-00143-1

Figure Lengend Snippet: Fig. 1 The levels of EGC biomarkers are significantly increased by HA conditions. a Serum concentrations of GFAP, S100β, GDNF, and NGF in control and HA group participants. b Relative mRNA expression per β-Actin of GFAP, S100β, GDNF, and NGF-β in the small intestines of control and HA group mice. c Immunohistochemical staining of the small intestine for GFAP and S100β. (n = 6–8 mice/group), Mean ± SD represent the findings. ****p < 0.0001, **p < 0.01, *p < 0.05. MOD—Mean Optical Density, IHC - immunohistochemistry

Article Snippet: To explore the role of S100β, MODE-K cells were treated with 5 μM recombinant mouse S100β (Solarbio, P00208) and subjected to hypoxia for 12 h, and control MODE-K cells were subjected to hypoxia alone.

Techniques: Control, Expressing, Immunohistochemical staining, Staining, Immunohistochemistry

Journal: Molecular biomedicine

Article Title: Enteric glial cells aggravate the intestinal epithelial barrier damage by secreting S100β under high-altitude conditions.

doi: 10.1186/s43556-023-00143-1

Figure Lengend Snippet: Fig. 5 S100β mediates the effect of EGCs to aggravate epithelial cell injury under hypoxic conditions. a Effect of exogenous S100β on MODE-K epithelial cell proliferation under hypoxic conditions. b Representative flow cytometric plots of MODE-K cell apoptosis. Annexin V and PI were used to label the cells before they were analyzed by flow cytometry. The figures show what proportion of the total occur in each quadrant. c Statistical analysis of the frequency percentage in late-phase apoptosis. d Relative mRNA expression per β-Actin of IL-6, -10, -1α, -1β, and TNF-α, claudin-1, occludin, and ZO-1. e Occludin and ZO-1 protein expression. Representation of findings and significance as previously stated

Article Snippet: To explore the role of S100β, MODE-K cells were treated with 5 μM recombinant mouse S100β (Solarbio, P00208) and subjected to hypoxia for 12 h, and control MODE-K cells were subjected to hypoxia alone.

Techniques: Flow Cytometry, Expressing

Journal: Journal of Korean Neurosurgical Society

Article Title: S100ß, Matrix Metalloproteinase-9, D-dimer, and Heat Shock Protein 70 Are Serologic Biomarkers of Acute Cerebral Infarction in a Mouse Model of Transient MCA Occlusion

doi: 10.3340/jkns.2017.0200

Figure Lengend Snippet: Plasma S100β concentration in all groups. The concentration of S100β increases with occlusion time (p=0.001; A) and correlates significantly with infarct volume (r=0.867, p <0.001; b) and neurological deficit (r=0.802, p <0.001; c). * p <0.05.

Article Snippet: The plasma concentrations of S100β, MMP-9, D-dimer, and HSP70 were calculated using mouse protein S100β (CSB-EL-0206643MO; CUSABIO, Wuhan, China), mouse total MMP-9 (MMPT90; R&D Systems, Minneapolis, MN, USA), mouse D-dimer (E03D0224; BlueGene, Shanghai, China), and mouse HSP70 (CSB-E08311m; CUSABIO) ELISA kits.

Techniques: Clinical Proteomics, Concentration Assay

Journal: Journal of Korean Neurosurgical Society

Article Title: S100ß, Matrix Metalloproteinase-9, D-dimer, and Heat Shock Protein 70 Are Serologic Biomarkers of Acute Cerebral Infarction in a Mouse Model of Transient MCA Occlusion

doi: 10.3340/jkns.2017.0200

Figure Lengend Snippet: Sensitivity and specificity of the biomarkers. MMP-9 and HSP70 both have an AUc of 1. S100β has an AUc of 0.98. The AUc for D-dimer is 0.58. MMP-9 : matrix metalloproteinase-9, HSP70 : heat shock protein 70, AUc : the area under the receiver operating characteristic curve.

Article Snippet: The plasma concentrations of S100β, MMP-9, D-dimer, and HSP70 were calculated using mouse protein S100β (CSB-EL-0206643MO; CUSABIO, Wuhan, China), mouse total MMP-9 (MMPT90; R&D Systems, Minneapolis, MN, USA), mouse D-dimer (E03D0224; BlueGene, Shanghai, China), and mouse HSP70 (CSB-E08311m; CUSABIO) ELISA kits.

Techniques: