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Image Search Results
Journal: Communications Biology
Article Title: Intrinsic cardiac adrenergic cells contribute to LPS-induced myocardial dysfunction
doi: 10.1038/s42003-022-03007-6
Figure Lengend Snippet: a Co-immunofluorescent staining of TLR4 and TH in NRVM ICA cell+ , TLR4: toll-like receptor 4, red; TH: ICA cells, green; DAPI: nuclei, blue ( n = 6). b and c NE production as well as TH and DBH expression in rat ICA cells treated with Viper (TLR4 inhibitor, 10 μM) for 2 h prior to LPS for 6 h. ( n = 48, each dot represents one independent repeat). d TLR4 expression in wildtype (WT) and TLR4-deficient ( Tlr4 Lps-del ) NMVM ICA cell+ . e and f NE production and DBH expression in WT and Tlr4 Lps-del NMVM ICA cell+ stimulated with LPS for 6 h, control: saline ( n = 12, each dot represents a biological replicate in d – f ). g Luciferase activity of AP-1-luc- and TH-promoter-luc- relative to RLTK-luc- in HEK293/hTLR4 cells at 36 h after transfection and LPS stimulation. h Luciferase activity of AP-1-luc- and TH-promoter-luc- relative to RLTK-luc- in HEK293/hTLR4 cells at 24 h after transfection with plasmids (0.1 μg/mL) encoding MyD88 and TRIF. i Expression of c-Jun and c-Fos in HEK293/hTLR4 cells at 24 h after transfection with MyD88 plasmid, c-Jun siRNA and c-Fos siRNA. j Luciferase activity of TH-promoter-luc- relative to RLTK-luc- in HEK293/hTLR4 cells at 24 h after transfection with MyD88 plasmid, c-Jun siRNA, and c-Fos siRNA, (0.1 μg/mL for plasmid) (each dot represents one independent repeat in ( g – j )). Data are presented as mean ± SEM using one-way ANOVA and Bonferroni multiple comparison test, * P < 0.05, ** P < 0.01, most of the P -values were assigned on the figure. n represents the number of neonatal rats ( a – c ) or neonatal mice ( d – f ).
Article Snippet: α 1 -AR antagonist: Prazosin (Sigma-Aldrich#7791); α 2 -AR antagonist: Yohimbine (Sigma-Aldrich #Y3125); α 2A -AR antagonist: BRL 44408 (Sigma-Aldrich #B4559); β 1 -AR antagonist: CGP20712A (Sigma-Aldrich #C231); β 2 -AR antagonist: ICI-118 551 (Sigma-Aldrich #I127); β 3 -AR antagonist: SR59230A (Sigma-Aldrich #S8688);
Techniques: Staining, Expressing, Control, Saline, Luciferase, Activity Assay, Transfection, Plasmid Preparation, Comparison
Journal: Communications Biology
Article Title: Intrinsic cardiac adrenergic cells contribute to LPS-induced myocardial dysfunction
doi: 10.1038/s42003-022-03007-6
Figure Lengend Snippet: ICA cell produces no TNF-α due to the elevated Nfkbia and Tnfaip6 expression. Increased NE release by LPS-TLR4 signaling activates β1-AR-CaMKII signaling in cardiomyocytes to regulate NF-κB and mitogen-activated protein kinase pathways, subsequently aggravating myocardial TNF-α production and dysfunction.
Article Snippet: α 1 -AR antagonist: Prazosin (Sigma-Aldrich#7791); α 2 -AR antagonist: Yohimbine (Sigma-Aldrich #Y3125); α 2A -AR antagonist: BRL 44408 (Sigma-Aldrich #B4559); β 1 -AR antagonist: CGP20712A (Sigma-Aldrich #C231); β 2 -AR antagonist: ICI-118 551 (Sigma-Aldrich #I127); β 3 -AR antagonist: SR59230A (Sigma-Aldrich #S8688);
Techniques: Expressing