Skip to main content
. 2020 Feb 6;32:101453. doi: 10.1016/j.redox.2020.101453

Fig. 1.

Fig. 1

Cardiac Tsg101 expression is altered during development and upon oxidative stress. (A) Representative immunoblots and quantitative analyses showing protein levels of Tsg101 in cardiac lysates extracted from postnatal day (P) 1 (P1), P7, P21 and adult (2-month old, male) mice (FVB/N). *, p < 0.05 vs. P1. (B) Representative immunoblots and quantitative analyses showing protein levels of Tsg101 in cardiomyocytes isolated from neonates (P1) and adult (2-month old, male) mice (FVB/N). *, p < 0.05 vs. neonates. (C) Representative immunoblots and quantitative analysis showing protein levels of Tsg101 in 2-month old mouse (FVB/N, male) hearts subjected to ex vivo 30-min, 45-min or 1-h global ischemia followed by 1-h reperfusion. *, p < 0.05 vs. pre-I/R samples. (D) Representative immunoblots and quantitative analyses revealing protein levels of Tsg101 in 2-month old mouse (FVB/N, male) hearts subjected to in vivo 30-min or 1-h ischemia followed by 4-h reperfusion. *, p < 0.05 vs. Sham-operated samples. (e) Representative immunoblots and quantitative analysis showing protein levels of Tsg101 in adult Sprague Dawley rat (4–5 week old, male) cardiomyocytes treated with PBS or H2O2 (100 μM) for 1 h *, p < 0.05 vs. PBS. GAPDH or α-Actin was used as a loading control.