Journal: Clinical Science (London, England : 1979)

Article Title: Paternal long-term PM 2.5 exposure causes hypertension via increased renal AT 1 R expression and function in male offspring

doi: 10.1042/CS20210802

Figure Lengend Snippet: ( A and B ) The mRNA (A) and protein expression (B) of AT 1 R were determined by qt-PCR and immunoblotting in the 12-week-old PM 2.5 offspring. AT 1 R mRNA level was normalized using GAPDH. The protein expression of AT 1 R was normalized using tubulin expression (A and B, two-tailed, unpaired t test, * P < 0.05 vs. control, n = 6). ( C ) Effect of losartan (20 mg/kg/d, 4 weeks) on the systolic blood pressure (SBP) in the PM 2.5 offspring (two-way ANOVA with Tukey’s post hoc test, * P < 0.05 vs. P- offspring +losartan, n = 8; # P < 0.05 vs. C-offspring, n = 8). ( D and E ) Effect of losartan (20 mg/kg/d, 4 weeks) on the 24 h urine volume (D) and sodium excretion (E) in the PM 2.5 offspring. (D and E, two-way ANOVA with Tukey’s post hoc test, * P < 0.05 vs. C-offspring, n = 8; # P < 0.05 vs. P-offspring, n = 8). ( F and G ) The mRNA (F) and protein expression (G) of GRK4 were determined by qt-PCR and immunoblotting in the 12-week-old PM 2.5 offspring. AT 1 R mRNA level was normalized using GAPDH. The protein expressions of GRK4 were normalized using tubulin expression (F and G, two-tailed, unpaired t test, * P < 0.05 vs. C-offspring, n = 6). Control offspring (C or C-offspring): offspring of vehicle-exposed paternal SD rats; PM 2.5 offspring (P or P-offspring): offspring of PM 2.5 -exposed paternal rats.

Article Snippet: The blots were subjected to immunoblot analyses with the primary polyclonal antibodies for rabbit anti-AT 1 R (1:1000; Proteintech Group, Rosemont, IL, U.S.A.), anti-GRK4 (1:500; Abcam, Cambridge, U.K.), anti-GAPDH (1:1000; Beyotime, Shanghai, China) and for mouse anti-tubulin (1:1000; Beyotime, Shanghai, China) overnight at 4°C.

Techniques: Expressing, Western Blot, Two Tailed Test

Journal: Clinical Science (London, England : 1979)

Article Title: Paternal long-term PM 2.5 exposure causes hypertension via increased renal AT 1 R expression and function in male offspring

doi: 10.1042/CS20210802

Figure Lengend Snippet: ( A and B ) Renal MDA (A) and SOD (B) levels were measured in vehicle (control)- and PM 2.5 -treated paternal SD rats (A and B, two-tailed, unpaired t test, * P < 0.05 vs. control, n = 6). ( C–E ) Systolic blood pressure (SBP) ( C ), 24 h urine volume ( D ) and sodium excretion ( E ) were determined in the 12-week-old offspring of 12 weeks PM 2.5 -exposed- and 16 weeks tempol-treated paternal rats (C–E: two-way ANOVA with Tukey’s post hoc test, * P < 0.05 vs. control offspring, n = 8; # P < 0.05 vs. PM 2.5 offspring, n = 8). ( F and G ) Protein expressions of AT 1 R (F) and GRK4 (G) were determined by Western blot in the kidney from the 12-week-old offspring of 12 weeks PM 2.5 -exposed- and 16 weeks tempol-treated paternal rats. AT 1 R or GRK4 protein expression was normalized using GAPDH expression (F and G, two-way ANOVA with Tukey’s post hoc test, * P < 0.05 vs. control, n = 6; # P < 0.05 vs. PM 2.5 , n = 6). Control: vehicle-exposed paternal rats; PM 2.5 : PM 2.5 -exposed-paternal rats; C-offspring: offspring of vehicle-exposed and vehicle-treated paternal rats; P-offspring: offspring of PM 2.5 -exposed and vehicle-treated paternal rats; C+Tempol-offspring: offspring of vehicle-exposed- and tempol-treated paternal rats; P+Tempol-offspring: offspring of PM 2.5 -exposed- and tempol-treated paternal rats.

Article Snippet: The blots were subjected to immunoblot analyses with the primary polyclonal antibodies for rabbit anti-AT 1 R (1:1000; Proteintech Group, Rosemont, IL, U.S.A.), anti-GRK4 (1:500; Abcam, Cambridge, U.K.), anti-GAPDH (1:1000; Beyotime, Shanghai, China) and for mouse anti-tubulin (1:1000; Beyotime, Shanghai, China) overnight at 4°C.

Techniques: Two Tailed Test, Western Blot, Expressing

Journal: Clinical Science (London, England : 1979)

Article Title: Paternal long-term PM 2.5 exposure causes hypertension via increased renal AT 1 R expression and function in male offspring

doi: 10.1042/CS20210802

Figure Lengend Snippet: Paternal PM 2.5 exposure, via increased oxidative stress, elevates renal expressions of GRK4 and its downstream target AT 1 R in their offspring, which leads to the enhanced AT 1 R-mediated urinary sodium retention, and ultimately hypertension.

Article Snippet: The blots were subjected to immunoblot analyses with the primary polyclonal antibodies for rabbit anti-AT 1 R (1:1000; Proteintech Group, Rosemont, IL, U.S.A.), anti-GRK4 (1:500; Abcam, Cambridge, U.K.), anti-GAPDH (1:1000; Beyotime, Shanghai, China) and for mouse anti-tubulin (1:1000; Beyotime, Shanghai, China) overnight at 4°C.

Techniques:

Journal: Pulmonary pharmacology & therapeutics

Article Title: Neutralization of both IL-1α/IL-1β plays a major role in suppressing combined cigarette smoke/virus-induced pulmonary inflammation in mice.

doi: 10.1016/j.pupt.2017.03.008

Figure Lengend Snippet: Fig. 1. Target engagement for IL-1a, IL-1b and IL-1R1 Abs. (A) Mice were treated i.p. with (B) IL-1R1 (#JAMA-147) antibodies (Abs) or (C) IL-1a (#ALF-161) or IL-1b (#315B4G5) Abs 18 h prior to i.t. administration of 10 ng recombinant mouse IL-1a or IL-1b. Amount of Ab per mouse was adjusted by administration of the corresponding isotype controls as described in material and methods. Phosphorylated ERK was measured in lung homogenate 20 min after administration of the stimulus. Mean values ± SEM of n ¼ 4 mice are shown. ***p < 0.001, **p < 0.01 represent significant differences compared to the positive control group.

Article Snippet: Abs against mouse IL-1a (clone ALF-161, haIgG, eBioscience, USA) and mouse IL-1R1 (clone JAMA-147, haIgG, BioXCell, USA) were sourced commercially, as well as the isotype control Ab eBio299Arm (haIgG, eBioscience, USA).

Techniques: Drug discovery, Recombinant, Positive Control

Journal: Pulmonary pharmacology & therapeutics

Article Title: Neutralization of both IL-1α/IL-1β plays a major role in suppressing combined cigarette smoke/virus-induced pulmonary inflammation in mice.

doi: 10.1016/j.pupt.2017.03.008

Figure Lengend Snippet: Fig. 4. Treatment of CS-exposed and H1N1-infected mice with IL-1R1 Ab or combined IL-1a/IL-1b Abs. (A) As described in the legend of Fig. 2, mice were exposed to cigarette smoke (CS) for a total of nine days and infected with influenza virus (H1N1) on day 8. Mice were treated with an antibody (Ab) targeting IL-1R1 or a combination of Abs targeting IL-1a/IL- 1b and adjusted with isotype control Abs. (B) Body-weight loss is displayed as time course and as % change at day 12 compared to day 1. (C) Total cells, (D) neutrophils and (E) macrophages in BAL fluid are illustrated. Mean values ± SEM of n ¼ 7e8 mice are shown. ***p < 0.001, *p < 0.05 represent significant differences compared to the CS/H1N1 group or the IL-1R1 group, respectively. The inhibitory activity of the treatments is reported as % inhibition of CS/H1N1 over baseline (negative control group).

Article Snippet: Abs against mouse IL-1a (clone ALF-161, haIgG, eBioscience, USA) and mouse IL-1R1 (clone JAMA-147, haIgG, BioXCell, USA) were sourced commercially, as well as the isotype control Ab eBio299Arm (haIgG, eBioscience, USA).

Techniques: Infection, Virus, Control, Activity Assay, Inhibition, Negative Control

Journal: Pulmonary pharmacology & therapeutics

Article Title: Neutralization of both IL-1α/IL-1β plays a major role in suppressing combined cigarette smoke/virus-induced pulmonary inflammation in mice.

doi: 10.1016/j.pupt.2017.03.008

Figure Lengend Snippet: Fig. 5. Detection of H1N1 and gene expression analysis of ICAM-1 and MUC5A/C. Mice were exposed to cigarette smoke (CS) for a total of nine days and infected with influenza virus (H1N1) on day 8. Mice were treated with antibodies (Abs) as described before. qPCR was used for detection of (A) viral genomes and for gene expression analysis of (B) MUC5A/C and (C) ICAM-1 as described in material and methods. DCT-values are illustrated. Mean values ± SEM of n ¼ 7e8 mice are shown. ***p < 0.001, **p < 0.01, *p < 0.05 represent significant differences compared to the CS/H1N1 group or the IL-1R1 group, respectively.

Article Snippet: Abs against mouse IL-1a (clone ALF-161, haIgG, eBioscience, USA) and mouse IL-1R1 (clone JAMA-147, haIgG, BioXCell, USA) were sourced commercially, as well as the isotype control Ab eBio299Arm (haIgG, eBioscience, USA).

Techniques: Gene Expression, Infection, Virus