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Mitochondrial permeability transition pore (mPTP) opening is a terminal event leading to mitochondrial dysfunction and cell death under conditions of oxidative stress (OS). However, mPTP blockade with cyclosporine A (CsA) has shown variable efficacy in limiting post-ischemic dysfunction and arrhythmias. We hypothesized that strong feedback between energy dissipating (mPTP) and cardioprotective (mKATP) channels determine vulnerability to OS.', 'Guinea pig hearts (N = 61) were challenged with H2O2 (200 μM) to elicit mitochondrial membrane potential (ΔΨm) depolarization. High-resolution optical mapping was used to measure ΔΨm or action potentials (AP) across the intact heart. Hearts were treated with CsA (0.1 μM) under conditions that altered the activity of mKATP channels either directly or indirectly via its regulation by protein kinase C. mPTP blockade with CsA markedly blunted (P < 0.01) OS-induced ΔΨm depolarization and delayed loss of LV pressure (LVP), but did not affect arrhythmia propensity. Surprisingly, prevention of mKATP activation with the chemical phosphatase BDM reversed the protective effect of CsA, paradoxically exacerbating OS-induced ΔΨm depolarization and accelerating arrhythmia onset in CsA treated compared to untreated hearts (P < 0.05). To elucidate the putative molecular mechanisms, mPTP inhibition by CsA was tested during conditions of selective PKC inhibition or direct mKATP channel activation or blockade. Similar to BDM, the specific PKC inhibitor, CHE (10 μM) did not alter OS-induced ΔΨm depolarization directly. However, it completely abrogated CsA-mediated protection against OS. Direct pharmacological blockade of mKATP, a mitochondrial target of PKC signaling, equally abolished the protective effect of CsA on ΔΨm depolarization, whereas channel activation with 30 μM Diazoxide protected against ΔΨm depolarization (P < 0.0001). Conditions that prevented mKATP activation either directly or indirectly via PKC inhibition led to accelerated ΔΨm depolarization and early onset of VF in response to OS. Investigation of the electrophysiological substrate revealed accelerated APD shortening in response to OS in arrhythmia-prone hearts.
Do functional crosstalk between the mitochondrial PTP and KATP channels determine arrhythmic vulnerability to oxidative stress?

P53 is a key protein which controls cell cycle arrest and apoptosis in response to DNA damage. Auto-antibodies against p53 have been detected in some cancer patients and also in patients with autoimmune diseases. In these patients, the main cause of anti-p53 antibody occurrence was considered to be increased intracellular p53 protein in cancer cells and autoreactive lymphocytes, respectively. Intracellular p53 also increases with cardiomyocyte apoptosis during heart failure and autoreactive lymphocytes play a role in the course of idiopathic dilated cardiomyopathy (IDC) and ischemic cardiomyopathy (ICM). Based on these observations, we hypothesized that anti-p53 antibody response may also occur in patients with heart failure due to ICM and IDC.', 'The aim of this study was to evaluate anti-p53 antibodies in the serum of patients with heart failure due to IDC and ICM.', '70 eligible patients with heart failure and severe left ventricular systolic dysfunction (mean fractional shortening 12.03 +/- 3.93%) were included in the study. The aetiology of heart failure was IDC in 26 patients and ICM in 44 patients, according to the angiographic and echocardiographic findings.', 'Anti-p53 antibodies were not detected in any of the patients.
Do serum anti-p53 antibodies occur in patients with heart failure due to idiopathic dilated and ischemic cardiomyopathies?

To demonstrate the feasibility of in vivo monitoring of the myogenic differentiation process from human muscle precursor cells to mature skeletal muscle tissue by measuring characteristic magnetic resonance (MR) imaging relaxation and diffusion properties as a potential noninvasive diagnostic tool in muscle cell therapy.', 'The study was approved by the ethics committee for studies in humans and the animal care committee. The hypothesis was tested by means of subcutaneous injection of human muscle precursor cells from the rectus abdominis muscle into nude mice (n = 18). Animals injected with human fibroblasts, prostate cancer cells, or collagen served as control animals (four in each group). T1, T2, T2*, and apparent diffusion coefficients (ADCs) were measured at 4.7-T MR imaging. MR imaging parameters were statistically evaluated by using analysis of variance with Bonferroni correction. The engineered muscle was characterized by means of immunofluorescence, Western blot, and contraction assays.', 'Muscle tissue in the early stages of the differentiation process exhibited distinctly higher T1 (mean ± standard deviation, 2242 msec ± 116), T2 (224 msec ± 18), and T2* (33.3 msec ± 3.6) values and ADCs (1.53 × 10(-3) mm(2)/sec ± 0.03) compared with those of skeletal muscle. The muscle precursor cells exhibited a nonspecific pattern compared with that in control animals in the early stages. During differentiation, the relaxation and diffusion parameters decreased and approached the values for mature skeletal muscle tissue: T1, 1386 msec ± 88; T2, 32.0 msec ± 4.3; T2*, 10.8 msec ± 0.8; ADC, 1.39 × 10(-3) mm(2)/sec ± 0.02 (reference erector spinae muscle tissue: T1, 1417 msec ± 106; T2, 31.0 msec ± 2.4; T2*, 11.3 msec ± 1.7; and ADC, 1.40 × 10(-3) mm(2)/sec ± 0.03).

Does mR imaging relaxometry allow noninvasive characterization of in vivo differentiation of muscle precursor cells?