Display Settings:

Items per page
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information

Results: 6

1.
Fig. 3.

Fig. 3. From: Cardioprotective effects of thioredoxin in myocardial ischemia and the reperfusion role of S-nitrosation.

Antiapoptotic effects of Trx and enhancement by S-nitrosation. (A) Effect of hTrx and its S-nitrosated form (hTrx-SNO) on postischemic myocardial apoptosis as assessed by TUNEL-positive myocytes. (B) Effect of hTrx and S-nitrosated hTrx on postischemic myocardial apoptosis as assessed by caspase-3 activity. **, P < 0.01 vs. vehicle group; ##, P < 0.01 vs. MI/R treated with native hTrx.

Ling Tao, et al. Proc Natl Acad Sci U S A. 2004 August 3;101(31):11471-11476.
2.
Fig. 5.

Fig. 5. From: Cardioprotective effects of thioredoxin in myocardial ischemia and the reperfusion role of S-nitrosation.

Incubation of eTrx with GSNO neither causes appreciable protein S-nitrosation (A) nor potentiates its antiapoptotic effect as determined by TUNEL staining (B) and caspase-3 activity (C). **, P < 0.01 vs. vehicle group. Means ± SEM of 10-12 mice per group.

Ling Tao, et al. Proc Natl Acad Sci U S A. 2004 August 3;101(31):11471-11476.
3.
Fig. 2.

Fig. 2. From: Cardioprotective effects of thioredoxin in myocardial ischemia and the reperfusion role of S-nitrosation.

S-Nitrosation of hTrx as measured by chemiluminescence and Western blotting. (A) Extent of S-nitrosation after preincubation of hTrx with increasing concentrations of GSNO as quantified by gas phase chemiluminescence (means ± SEM, n = 3, hTrx, 16.7 μM). (B) Representative Western blots using a Nitro-Glo kit (to detect S-nitrosated protein, Upper) or using an anti-hTrx antibody as primary antibody (to detect hTrx, Lower). Lanes: 1, GSNO-treated hTrx; 2, vehicle-treated hTrx; 3, molecular marker.

Ling Tao, et al. Proc Natl Acad Sci U S A. 2004 August 3;101(31):11471-11476.
4.
Fig. 4.

Fig. 4. From: Cardioprotective effects of thioredoxin in myocardial ischemia and the reperfusion role of S-nitrosation.

Myocardial infarct size in the different treatment groups. (Upper) Representative photomicrographs of heart sections obtained from mice subjected to sham myocardial ischemia/reperfusion (MI/R), MI/R treated with vehicle, MI/R treated with native hTrx, or S-nitrosated hTrx. Blue portion, nonischemic, normal region; red portion, ischemic/reperfused, but not infarcted region; negatively stained portion, ischemic/reperfused, infarcted region. (Lower) Bar chart of myocardial infarct size expressed as percent of total ischemic/reperfused area (area-at-risk; means ± SEM of 10-12 mice per group). **, P < 0.01 vs. vehicle-treated ischemic/reperfused hearts; ##, P < 0.01 vs. hTrx.

Ling Tao, et al. Proc Natl Acad Sci U S A. 2004 August 3;101(31):11471-11476.
5.
Fig. 6.

Fig. 6. From: Cardioprotective effects of thioredoxin in myocardial ischemia and the reperfusion role of S-nitrosation.

Potential mechanisms responsible for the cardioprotective effects on hTrx and its modification by S-nitrosation. (A) Effect of hTrx on ischemia/reperfusion-induced p38 MAPK activation and its modification by S-nitrosation. (Upper) Representative Western blot of phosphorylated ATF-2. (Lower) Quantitative densitometry of ≥5 independent experiments. **, P < 0.01 vs. MI/R plus vehicle; ##, P < 0.01 vs. MI/R plus hTrx. (B) Representative Western blots of S-nitrosated proteins from sham MI/R (lanes 1 and 2), MI/R plus vehicle (lanes 3 and 4), MI/R plus hTrx (lanes 5 and 6), and MI/R plus hTrx-SNO (lanes 7 and 8) as detected with a Nitro-Glo kit. An identical amount of protein was loaded on each lane (20 μg per lane).

Ling Tao, et al. Proc Natl Acad Sci U S A. 2004 August 3;101(31):11471-11476.
6.
Fig. 1.

Fig. 1. From: Cardioprotective effects of thioredoxin in myocardial ischemia and the reperfusion role of S-nitrosation.

Effect of hTrx on postischemic myocardial apoptosis. (A) Representative photograph of electrophoretic analysis of internucleosomal DNA extracted from sham-operated control hearts (S) or mouse hearts exposed to I/R receiving either vehicle (V) or hTrx. (B) Representative photographs of TUNEL staining. Nuclei of normal cells are stained blue, and apoptotic nuclei are stained red. (C) Summary of TUNEL-positive myocytes from 8-10 mice per group. Assays were performed in a blinded fashion. (D) Summary of caspase-3 activity determined with a colorimetric assay kit. n = 10-12 per group. **, P < 0.01 vs. vehicle group. (E) Representative photographs of hTrx immunostaining confirming uptake of hTrx by cardiomyocytes.

Ling Tao, et al. Proc Natl Acad Sci U S A. 2004 August 3;101(31):11471-11476.

Display Settings:

Items per page

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk