milk mouse monoclonal antibody anti il6 santa cruz biotechnology sc57315  (Santa Cruz Biotechnology)

Journal: Stem Cell Research & Therapy

Article Title: The treatment of acute tendon injury with small extracellular vesicles originating from TNFAIP6 − ADSCs subpopoulation both in vitro and in vivo

doi: 10.1186/s13287-025-04789-2

Figure Lengend Snippet: Let-7c-5p inhibits inflammatory expression in tendon injury. A The expression of CCR7 + , CD163 + , IL-6 + , and IL-10 + cells were detected by immunofluorescence at week 1. B Positive ratio of inflammation-related factors ( n = 6). Bars 50 μm. Data are represented as mean ± SD. *vs Control group; # vs. ADSC-sEVs; n = 6. * P < 0.05, ** P < 0.01, # P < 0.05, ## P < 0.01, ### P < 0.001

Article Snippet: For immunofluorescence analysis, tissue sections were incubated with primary antibodies: anti-CCR7 (ab32527; Abcam), anti-CD163 (ab182422; Abcam), anti-interleukin (IL)-6 (TA500067S; Origene), and anti-IL-10 ( ab33471; Abcam), followed by incubation with secondary antibodies (SA00013; ProteinTech, Chicago, IL, USA).

Techniques: Expressing, Immunofluorescence, Control

Journal: Brain sciences

Article Title: Enhanced Interleukin 6 Trans-Signaling Modulates Disease Process in Amyotrophic Lateral Sclerosis Mouse Models.

doi: 10.3390/brainsci15010084

Figure Lengend Snippet: Figure 1. Generation of unique knock-in mouse model C57BL/6 Il6raE357A and IL6R transmembrane deletion (TMD) mouse models. To accurately investigate the potential mechanisms by which IL6 trans-signaling contributes to disease progression, it was necessary to generate a knock-in mouse model C57BL/6 Il6raE357A of IL6 trans-signaling. The mouse Il6ra gene was altered by incorporating a two-base-pair change (AA > CT) at the codon for amino acid 357, thus converting the Glu357 (GAA) to Ala357 (GCT) (A,B). Incorporating this codon change also produced a novel Hind III site that allows us to identify mice heterozygous (HT) or homozygous (HM) for the E357A allele (B). ELISA measurement of soluble IL6 receptor in (C) Il6raE357A mice at P90 (Ala/Ala n = 13; Ala/Glu n = 35; Glu/Glu n = 19; p < 0.001 across genotypes; one-way ANOVA) confirmed increased concentrations of soluble receptor in serum. We also created a unique IL6R transmembrane deletion (TMD) mouse model that exhibits tremendous shedding of the receptor (D). ELISA measurements of soluble IL6 receptor in Il6raTMD mice at P90 (TMD/TMD n = 17; WT/WT n = 16; p < 0.001 across genotypes; one-way ANOVA) are plotted (E). ELISA measurements of plasma IL6 in untreated or LPS-treated (3 ug/g, i.p) WT, E357A homozygous and TMD homozygous mice at indicated time points (F). For each treatment group, P90 sex-matched, littermate WT and Il6ra littermates were used. Littermate, gender-matched animals were used (n = 2–3 groups/treatment group/time point). (G) Shown are representative Western blots of untreated or LPS-treated WT, E357A homozygous (HM) and TMD homozygous liver protein extracts 2 and 24 h after LPS administration. Littermate, gender-matched animals were used per treatment group/time point (liver, brain n = 3; kidney n = 2). Phosphorylated Stat3 and total Stat3 levels were normalized to Hsc70 used as a loading control and the ratio of P-Stat3/total Stat3 determined for each tissue sample. Results are expressed as fold-change in Il6ra over WT littermate. Phosphorylated Stat3 expression increased by 2 h in all animals but was greater in the il6ra models, a pattern observed at 24 h.

Article Snippet: InVivoMAb anti-mouse Il6ra15A7 monoclonal antibody reacts with the mouse IL6 receptor and inhibits IL6 from binding (manufacturer’s data, BioXcell, Lebanon, NH, USA, #BE0047) [28].

Techniques: Knock-In, Biomarker Discovery, Produced, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Western Blot, Control, Expressing

Journal: Brain sciences

Article Title: Enhanced Interleukin 6 Trans-Signaling Modulates Disease Process in Amyotrophic Lateral Sclerosis Mouse Models.

doi: 10.3390/brainsci15010084

Figure Lengend Snippet: Figure 6. To begin to investigate if there is a specific, IL6 trans-signaling-mediated glial response and if spinal MNs have unique responses in conditions of trans-signaling, we used a discovery-level whole transcriptome-based spatial RNAseq analysis of the ventral, lateral lumbar spinal cord of SOD1 and SOD1 X Il6raTMD mice. The overall cytoarchitecture and cells exhibiting MN phenotypes were identified by H&E staining and the image capture of sections prior to RNA isolation (A). (B) Individual 55 um diameter analysis spots containing MNs were identified by the expression of the mnx1 (HB9; [38]) and mnx1-negative, GFAP and/or Aif1 (IBA1) surrounding glial spots selected (C–E). (F) Photomicrograph of an adjacent spinal cord section processed by double-label immunofluorescence for ChAT to identify MNs (red) and GFAP to identify astrocytes (green) in the same MN-enriched region as shown in (A) (arrows in (A,F)). (G) The enhanced volcano plot indicates the extent of differential gene expression between MNs of SOD1 vs. SOD1 X Il6raE357A mice. (H) Pathway analysis was performed and identified IL6 trans-signaling-specific pathways associated with glial responses at P80 in SOD1 X Il6raTMD mice.

Article Snippet: InVivoMAb anti-mouse Il6ra15A7 monoclonal antibody reacts with the mouse IL6 receptor and inhibits IL6 from binding (manufacturer’s data, BioXcell, Lebanon, NH, USA, #BE0047) [28].

Techniques: Staining, Isolation, Expressing, Immunofluorescence, Gene Expression