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Fig. 2. Overexpressed and internalized S100A1 enhance cytosolic Ca²⁺-turnover in neonatal ventricular cardiomyocytes. (A-D) Adenoviral-transduced NVCMs overexpressing S100A1. (A) Superimposed tracings of calibrated Ca²⁺-transients in S100A1-overexpressing (AdS100A1, solid line) and control (Adcontrol, dashed line) NVCMs. Note the gain in systolic [Ca²⁺]_i in S100A1-overexpressing NVCMs (bar). (B-D) Effects of increased S100A1 protein level on Ca²⁺-transients. Compared with control cells expressing endogenous levels of S100A1, S100A1 overexpression significantly increases the Ca²⁺-transient amplitude (AdS100A1 454±22 nM vs. Adcontrol 311±11 nM; 1B), lowers diastolic [Ca²⁺]_i (AdS100A1 181±14 nM vs. Adcontrol 219±12 nM; 1C), and accelerates the decay of the Ca²⁺-transient (, AdS100A1 172±14 ms vs. Adcontrol 223±11 ms; 1D). n=150 cells from three different cell preparations. Data are given as mean±s.e.m. (A'-D') NVCMs treated with 1 µM human recombinant S100A1. (A') Superimposed tracings of calibrated Ca²⁺-transients in S100A1-treated (S100A1, solid line) and mock-treated (control, dashed line) NVCMs. The decrease in diastolic [Ca²⁺]_i in S100A1-treated NVCMs is indicated by the bar. (B') S100A1-uptake increases the Ca²⁺-transient amplitude (S100A1-treated 442±23 nM vs. control 324±15 nM). (C') The effects of an increased S100A1 level are a reduction of diastolic [Ca²⁺]_i (S100A1-treated 143±13 nM vs. control 236±14 nM) and (D') an accelerated decay of the Ca²⁺-transient (, S100A1-treated 182±16 ms vs. control 232±10 ms). Pre-incubation with monodansylcadaverine (MDC, an inhibitor of clathrin-mediated endocytosis) abolished the effects of extracellularly added S100A1 on the Ca²⁺-turnover (^* P<0.01 vs. no inhibitor).

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