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Bartolucci, C.

Publications and source records attributed to Bartolucci, C..

3 recordsLinked to original sources

RvD1 and LXA4 inhibitory effects on cardiac voltage-gated potassium channels

AimsThe resolution of inflammation is modulated by specialized pro-resolving lipid mediators (SPMs), which can be modified in some cardiovascular diseases. Among them, RvD1 and LXA4 prevent atrial fibrillation (AF) remodeling in the atria and cardiac hypertrophy, respectively in animal models. However, little is known about their electrophysiological effects on cardiac voltage-gated (VG) ion channels. Methods and resultsWe used the patch-clamp technique in heterologous systems and cardiomyocytes to assess the acute effect of RvD1, and LXA4, on VG potassium currents. In silico simulations were used to predict the effect of current modulation on the atrial and ventricular action potentials (AP). RvD1 and LXA4 reduced IKs (channel KV7.1/KCNE1) in COS-7 cells and guinea-pig cardiomyocytes without modifying its voltage dependence; RvD1 was more potent than LXA4. In heterologous systems, RvD1 was also tested on IKur (channel KV1.5), Ito (channel KV4.3/KChIP2), IKr (channel KV11.1), and IK1 (channel Kir2.1) with the largest inhibitory effect on IKs and IKr. In simulations RvD1 prolonged repolarization significantly in both atrial and ventricular myocytes. ConclusionThe results provide a comprehensive evaluation of RvD1 and LXA4 on cardiac human potassium channels, at pathophysiological relevant concentrations, being RvD1 more potent than LXA4. The predicted effects on the action potential suggest that, along with their antiinflammatory action, RvD1 may reverse AF-induced electrical remodeling in the atria by direct modulation of K+ currents. The same action might instead contribute to ventricular functional remodeling; however, direct evidence for this is missing.

pharmacology and toxicology↗

A novel ionic model for matured and paced atrial-like hiPSC-CMs integrating IKur and IKCa currents

Human induced pluripotent stem cells-derived cardiomyocytes have revolutionized the field of regenerative medicine, offering unparalleled potential for in-vitro modeling of normal and pathological human cardiomyocytes. The ability to produce stem cardiac myocytes in abundance has opened new avenues for drug efficacy and safety testing, as well as the study of conditions such as atrial fibrillation, a familial cardiac disorder. The development of atrial fibrillation is influenced by ion channel mutations, genetic variants, and other risk factors. Stem cells derived cardiomyocytes hold promise in personalized medicine, as they share the genetic heritage of the donor. While mathematical models have focused on immature stem cardiomyocytes phenotypes, they have primarily relied on a system of stiff ordinary differential equations. Computational modeling of diseased tissue presents an opportunity to evaluate drugs in a patient-specific manner, thereby improving therapeutic targets and ablation techniques. Previous studies categorized cell phenotypes based on action potential morphology, yet classification criteria remains ambiguous. This work introduces the first atrial-specific in-silico model of stem cells ionic currents, leveraging experimental data provided by Altomare et al. It begins by summarizing the baseline electrophysiological model and mathematical descriptions of atrial-specific additional currents. Model parameter tuning was performed through automatic optimization techniques to ensure realistic action potential shape and expedite the parameter adjustment process. The resulting model was validated against rate dependence and atrial-specific ion current blocking data. In summary, the development of an atrial-specific in-silico model represents a significant step forward in understanding cardiac electrophysiology and the potential for personalized medicine in treating conditions like atrial fibrillation. This model offers new tools for drug evaluation, therapeutic improvement, and a deeper comprehension of cardiac phenotypes. Author summaryHuman induced pluripotent stem cells have revolutionized regenerative medicine since their discovery in 2006, leading to a Nobel Prize in 2012. This kind of pluripotent cells can give rise to different types of specific tissue cells, such as derived cardiomyocytes. Differentiated cardiac cells offer an unlimited supply for studying human heart cells in normal and disease conditions, aiding a patient-specific drug testing and helping to explore pathogenic mechanisms behind different cardiomyopathies, including atrial fibrillation. Atrial fibrillation is a common heart condition, and stem cells with the same genetic heritage as the donor, are ideal for patient-specific treatments. Recent advances have produced mathematical models for the ionic currents in cardiomyocytes derived from stem cells, focusing on immature forms and enabling virtual drug testing. However, previous models did not capture the atrial-specific characteristics. We decided to create and introduce by this study the first atrial-like in-silico model for these cells, using novel experimental data. Thus, we describe the baseline model and additional atrial-specific currents, we tune the model parameters using automatic optimization technique, and we validate the models accuracy in simulating atrial action potentials and ion current blockage. This research paves the way for better understanding and treating atrial fibrillation and other heart conditions.

bioengineering↗

Coupling and Heterogeneity Modulate Pacemaking Capability in Healthy and Diseased Two-Dimensional Sinoatrial Node Tissue Models

Both experimental and modeling studies have attempted to determine mechanisms by which a small anatomical region, such as the sinoatrial node (SAN), can robustly drive electrical conduction in the human heart. However, despite important advances from prior research, important questions remain unanswered. This study aimed to investigate, through mathematical modeling, the role of intercellular coupling and cellular heterogeneity in synchronization and pacemaking within the healthy and diseased SAN. In a multicellular computational model of a monolayer of either human or rabbit SAN cells, simulations revealed that heterogenous cells synchronize their discharge frequency into a unique beating rhythm across a wide range of cellular heterogeneity and intercellular coupling. However, an insightful and unanticipated behavior appears in pathological conditions precipitated by perturbations of certain ionic currents (gCaL = 0.5): an intermediate range of intercellular coupling (900-4000 M{Omega}) is beneficial to the human SAN automaticity, enabling a very small portion of tissue (3.4%) to drive propagation, which fails with both lower and higher resistances. This protective effect of intercellular coupling and heterogeneity, seen in both human and rabbit tissues, highlights the remarkable resilience of the SAN. Overall, the model here developed allowed insight into the mechanisms of automaticity of the human sinoatrial node. The simulations suggest that certain degrees of gap junctional expressions protect the SAN from ionic perturbations that might be caused by drugs or mutations.

physiology↗