Priority Research Paper Volume 9, Issue 3 pp 627—649

Mitochondrial protein Fus1/Tusc2 in premature aging and age-related pathologies: critical roles of calcium and energy homeostasis

Figure 7CD. Fus1 KO cells show aberrant [Ca2+]c and [Ca2+]m responses to different stimuli that were improved by inhibiting the mitochondrial sodium/calcium exchanger (mNCX). (C) Steady state and LPS-induced [Ca2+]c profiles in WT and Fus1 KO MEFs. Panel I demonstrates major patterns of [Ca2+]c responses in WT and Fus1 KO primary MEFs at steady state and after LPS treatment detected by Fura-2 Ca2+-sensitive fluorescent dye. Panel II demonstrates the proportion of cells with Osc- and PL-type [Ca2+]c responses at steady state and after treatment with LPS (100 ng/mL). (D) Dynamics of basal, LPS- and CGP-induced [Ca2+]m responses in WT and KO primary MEFs. Panel I shows major patterns of [Ca2+]m responses at steady state and after LPS treatment (100 ng/mL) detected by MTG/Rhod-2 co-staining. Panel II shows the proportion of cells with SD-, SI-, and SS-patterns of [Ca2+]m responses in WT and Fus1 KO MEFs at steady state and after treatment with LPS (100 ng/mL). Panel III demonstrates the proportion of cells with SD-, SI-, and SS-patterns of [Ca2+]m responses after co-treatment of MEFs with LPS (100 ng/mL) and CGP37157 (CGP), an inhibitor of mitochondrial of Na+/Ca2+ exchanger. *p-value ≤ 0.05; **p-value ≤ 0.005 (Student's t-test, 2-sided unpaired). Data expressed as mean ± SEM.