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2 results on '"Nico Hartmann"'

1. Different activation of MAPKs and Akt/GSK3β after preload vs. afterload elevation

Author

Nico Hartmann, Lena Preuß, Belal A. Mohamed, Moritz Schnelle, Andre Renner, Gerd Hasenfuß, and Karl Toischer

Subjects
Hypertrophy, Preload, Afterload, AKT‐GSK3β, MAPKs, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Abstract Aims Pressure overload (PO) and volume overload (VO) lead to concentric or eccentric hypertrophy. Previously, we could show that activation of signalling cascades differ in in vivo mouse models. Activation of these signal cascades could either be induced by intrinsic load sensing or neuro‐endocrine substances like catecholamines or the renin‐angiotensin‐aldosterone system. Methods and results We therefore analysed the activation of classical cardiac signal pathways [mitogen‐activated protein kinases (MAPKs) (ERK, p38, and JNK) and Akt‐GSK3β] in in vitro of mechanical overload (ejecting heart model, rabbit and human isolated muscle strips). Selective elevation of preload in vitro increased AKT and GSK3β phosphorylation after 15 min in isolated rabbit muscles strips (AKT 49%, GSK3β 26%, P

Published
2022
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2. Inhibition of CaMKII Attenuates Progressing Disruption of Ca2+Homeostasis Upon Left Ventricular Assist Device Implantation in Human Heart Failure

Author

Samuel Sossalla, Nico Hartmann, Jörg Eiringhaus, Astrid Kleinwächter, Jonas Herting, Axel Haverich, Jan Gummert, André Renner, Thomas H. Fischer, and Jan D. Schmitto

Subjects
0301 basic medicine, medicine.medical_specialty, Cardiac output, medicine.medical_treatment, Biomedical Engineering, Diastole, Medicine (miscellaneous), Bioengineering, 030204 cardiovascular system & hematology, Biomaterials, 03 medical and health sciences, 0302 clinical medicine, Ca2+/calmodulin-dependent protein kinase, Internal medicine, medicine, Heart transplantation, business.industry, General Medicine, medicine.disease, Cardiac surgery, Surgery, 030104 developmental biology, Heart failure, Ventricular assist device, cardiovascular system, Cardiology, business, Homeostasis
Abstract

In heart failure, left ventricular assist device (LVAD) implantation is performed to ensure sufficient cardiac output. Whereas some patients are subsequently weaned from LVAD support, other patients still need heart transplantation. To elucidate underlying mechanisms, we assessed the arrhythmogenic SR-Ca(2+) leak at the time of LVAD implantation (HF-Im) and heart transplantation (HF-Tx) and evaluated the effects of CaMKII-inhibition. Human left-ventricular cardiomyocytes were isolated, paced at 1 Hz for 10 beats to ensure SR-Ca(2+) loading and scanned for diastolic Ca(2+) sparks (confocal microscopy). In HF-Im, the high diastolic spark frequency (CaSpF) of 0.76 ± 0.12 × 100 μm(-1) × s(-1) could be reduced to 0.48 ± 0.10 × 100 μm(-1) × s(-1) by CaMKII inhibition (AIP, 1 μM). The amplitude of Ca(2+) sparks, width, and length was not significantly altered. In sum, CaMKII inhibition yielded a clear tendency toward a reduction of the SR-Ca(2+) leak (n cells/patients = 76/6 vs. 108/6, P = 0.08). In HF-Tx, we detected an even higher CaSpF of 1.00 ± 0.10 100 μm(-1) × s(-1) and a higher SR-Ca(2+) leak compared with HF-Im (increase by 81 ± 33%, n cells/patients = 156/7 vs. 130/7, P

Published
2016

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