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. 2022 Dec 27;120(1):e2213537120. doi: 10.1073/pnas.2213537120

Fig. 2.

Fig. 2.

RGS7 mediates doxorubicin-induced mitochondrial dysfunction, oxidative stress, and cell death. (A) RGS7 immunoreactivity in total heart cultures treated with doxorubicin (n = 3; 3 μM, 16 h), 5-FU (n = 3; 500 mM, 16 h), or oxaliplatin (n = 3; 0.06 mM, 16 h). (B) Verification of RGS7 knockdown in total heart cultures with scramble or RGS7-shRNA (n = 4). (C–F) Control or RGS7 knockdown (KD) VCM were treated with doxorubicin ± pre-treatment of Ru360 (50 μM, 1 h) or cyclosporin A (0.2 mM, 45 min). (C) GPX activity (n = 5) and SOD activity (n = 5). (D) Mitochondrial Ca2+ flux (n = 5). (E) ΔψM (n = 5). (F) Apoptosis (cytoplasmic histone-associated DNA fragments; n = 5).