protein a hp spin trap affinity columns Search Results


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Intramyocardial injection of human extracellular vesicles (EVs) reduce activation of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome in a model of rat sterile pericarditis. (A) Schematic outline of the inflammatory effect of post operative pericarditis on NLRP3 activation, atrial remodeling and EV effects (red boxes). (B) Effect of pericarditis and EV treatment on the atrial content of NLRP3 and downstream mediators (interleukin-1 beta (IL-1β) and IL-18). NLRP3 data was analyzed using a one-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. talc + vehicle treated animals. Relationship between NLRP3 and IL-1β or IL-18 abundance within atrial tissue was analyzed using simple linear regression. (C) Rank order plot highlighting the abundance of miRNAs (left panel) and proteins (right panel) found in EVs suggested to directly inhibit NLRP3 activation. (D) In vitro effect of explant-derived cell (EDC) EVs on <t>caspase-1</t> activity, a measure of NLRP3 activation, in THP-1 cells (macrophages) and primary cultured atrial fibroblasts after activation by lipopolysaccharide (LPS) and nigericin. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. LPS+nigericin treated cells. (E) In vitro effect of EDC EVs on downstream mediators of NLRP3 activation (IL-1β and IL-18) in THP-1 cells (macrophages) after activation by LPS and nigericin. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. LPS+nigericin treated cells. (F) Comparative effect of EVs from bone marrow mesenchymal stromal cells (BM-MSCs), umbilical cord mesenchymal stromal cells (UC-MSCs) or EDCs on caspase-1 activity, the principal effector of NLRP3 activation. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. BM-MSC or UC-MSC treated cells. NEDD4, neural precursor cell expressed developmentally down-regulated protein 4; PRDX1, Peroxiredoxin-1; SQSTM1, Sequestosome 1.
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Becton Dickinson anti-maspin
Intramyocardial injection of human extracellular vesicles (EVs) reduce activation of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome in a model of rat sterile pericarditis. (A) Schematic outline of the inflammatory effect of post operative pericarditis on NLRP3 activation, atrial remodeling and EV effects (red boxes). (B) Effect of pericarditis and EV treatment on the atrial content of NLRP3 and downstream mediators (interleukin-1 beta (IL-1β) and IL-18). NLRP3 data was analyzed using a one-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. talc + vehicle treated animals. Relationship between NLRP3 and IL-1β or IL-18 abundance within atrial tissue was analyzed using simple linear regression. (C) Rank order plot highlighting the abundance of miRNAs (left panel) and proteins (right panel) found in EVs suggested to directly inhibit NLRP3 activation. (D) In vitro effect of explant-derived cell (EDC) EVs on <t>caspase-1</t> activity, a measure of NLRP3 activation, in THP-1 cells (macrophages) and primary cultured atrial fibroblasts after activation by lipopolysaccharide (LPS) and nigericin. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. LPS+nigericin treated cells. (E) In vitro effect of EDC EVs on downstream mediators of NLRP3 activation (IL-1β and IL-18) in THP-1 cells (macrophages) after activation by LPS and nigericin. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. LPS+nigericin treated cells. (F) Comparative effect of EVs from bone marrow mesenchymal stromal cells (BM-MSCs), umbilical cord mesenchymal stromal cells (UC-MSCs) or EDCs on caspase-1 activity, the principal effector of NLRP3 activation. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. BM-MSC or UC-MSC treated cells. NEDD4, neural precursor cell expressed developmentally down-regulated protein 4; PRDX1, Peroxiredoxin-1; SQSTM1, Sequestosome 1.
Anti Maspin, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Intramyocardial injection of human extracellular vesicles (EVs) reduce activation of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome in a model of rat sterile pericarditis. (A) Schematic outline of the inflammatory effect of post operative pericarditis on NLRP3 activation, atrial remodeling and EV effects (red boxes). (B) Effect of pericarditis and EV treatment on the atrial content of NLRP3 and downstream mediators (interleukin-1 beta (IL-1β) and IL-18). NLRP3 data was analyzed using a one-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. talc + vehicle treated animals. Relationship between NLRP3 and IL-1β or IL-18 abundance within atrial tissue was analyzed using simple linear regression. (C) Rank order plot highlighting the abundance of miRNAs (left panel) and proteins (right panel) found in EVs suggested to directly inhibit NLRP3 activation. (D) In vitro effect of explant-derived cell (EDC) EVs on caspase-1 activity, a measure of NLRP3 activation, in THP-1 cells (macrophages) and primary cultured atrial fibroblasts after activation by lipopolysaccharide (LPS) and nigericin. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. LPS+nigericin treated cells. (E) In vitro effect of EDC EVs on downstream mediators of NLRP3 activation (IL-1β and IL-18) in THP-1 cells (macrophages) after activation by LPS and nigericin. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. LPS+nigericin treated cells. (F) Comparative effect of EVs from bone marrow mesenchymal stromal cells (BM-MSCs), umbilical cord mesenchymal stromal cells (UC-MSCs) or EDCs on caspase-1 activity, the principal effector of NLRP3 activation. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. BM-MSC or UC-MSC treated cells. NEDD4, neural precursor cell expressed developmentally down-regulated protein 4; PRDX1, Peroxiredoxin-1; SQSTM1, Sequestosome 1.

Journal: Theranostics

Article Title: Inactivation of the NLRP3 inflammasome mediates exosome-based prevention of atrial fibrillation

doi: 10.7150/thno.89520

Figure Lengend Snippet: Intramyocardial injection of human extracellular vesicles (EVs) reduce activation of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome in a model of rat sterile pericarditis. (A) Schematic outline of the inflammatory effect of post operative pericarditis on NLRP3 activation, atrial remodeling and EV effects (red boxes). (B) Effect of pericarditis and EV treatment on the atrial content of NLRP3 and downstream mediators (interleukin-1 beta (IL-1β) and IL-18). NLRP3 data was analyzed using a one-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. talc + vehicle treated animals. Relationship between NLRP3 and IL-1β or IL-18 abundance within atrial tissue was analyzed using simple linear regression. (C) Rank order plot highlighting the abundance of miRNAs (left panel) and proteins (right panel) found in EVs suggested to directly inhibit NLRP3 activation. (D) In vitro effect of explant-derived cell (EDC) EVs on caspase-1 activity, a measure of NLRP3 activation, in THP-1 cells (macrophages) and primary cultured atrial fibroblasts after activation by lipopolysaccharide (LPS) and nigericin. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. LPS+nigericin treated cells. (E) In vitro effect of EDC EVs on downstream mediators of NLRP3 activation (IL-1β and IL-18) in THP-1 cells (macrophages) after activation by LPS and nigericin. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. LPS+nigericin treated cells. (F) Comparative effect of EVs from bone marrow mesenchymal stromal cells (BM-MSCs), umbilical cord mesenchymal stromal cells (UC-MSCs) or EDCs on caspase-1 activity, the principal effector of NLRP3 activation. One-way ANOVA with individual-mean comparisons by Šídák's multiple comparisons test. *P<0.05 vs. untreated cells; #P<0.05 vs. BM-MSC or UC-MSC treated cells. NEDD4, neural precursor cell expressed developmentally down-regulated protein 4; PRDX1, Peroxiredoxin-1; SQSTM1, Sequestosome 1.

Article Snippet: The specificity of caspase-1 activation was validated by including the caspase-1 inhibitor (YVAD-CHO, Promega).

Techniques: Injection, Activation Assay, Binding Assay, Sterility, In Vitro, Derivative Assay, Activity Assay, Cell Culture