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Difference between revisions of "Schleier 2020 J Cardiovasc Transl Res"

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(Created page with "{{Publication |title=Schleier Y, Moreno-Loaiza O, López Alarcón MM, Lopes Martins EG, Braga BC, Ramos IP, Galina A, Medei EH (2020) NOD mice recapitulate the cardiac disturb...")
 
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|year=2020
|year=2020
|journal=J Cardiovasc Transl Res
|journal=J Cardiovasc Transl Res
|abstract=This work aimed at testing the hypothesis that NOD/ShiLtJ mice (NOD) recapitulate the cardiac disturbances observed on type 1 diabetes (T1D). NOD mice were studied 4 weeks after the onset of hyperglycemia, and NOR/Lt mice matched as control. Cardiac function was evaluated by echocardiography and electrocardiography (ECG). Action potentials (AP) and Ca2+ transients were evaluated at whole heart level. Heart mitochondrial function was evaluated by high-resolution respirometry and H<sub>2</sub>O<sub>2</sub> release. NOD mice presented a reduction in hearth weight. Mitochondrial oxygen fluxes and H<sub>2</sub>O<sub>2</sub> release were similar between NOD and NOR mice. ECG revealed a QJ interval prolongation in NOD mice. Furthermore, AP duration at 30% of repolarization was increased, and it depicted slower Ca<sup>2+</sup> transient kinetics. NOD mice presented greater number/severity of ventricular arrhythmias both in vivo and ''in vitro''. In conclusion, NOD mice evoked cardiac electrical and calcium handling disturbances similar to the observed in T1D.
|abstract=This work aimed at testing the hypothesis that NOD/ShiLtJ mice (NOD) recapitulate the cardiac disturbances observed on type 1 diabetes (T1D). NOD mice were studied 4 weeks after the onset of hyperglycemia, and NOR/Lt mice matched as control. Cardiac function was evaluated by echocardiography and electrocardiography (ECG). Action potentials (AP) and Ca<sup>2+</sup> transients were evaluated at whole heart level. Heart mitochondrial function was evaluated by high-resolution respirometry and H<sub>2</sub>O<sub>2</sub> release. NOD mice presented a reduction in hearth weight. Mitochondrial oxygen fluxes and H<sub>2</sub>O<sub>2</sub> release were similar between NOD and NOR mice. ECG revealed a QJ interval prolongation in NOD mice. Furthermore, AP duration at 30% of repolarization was increased, and it depicted slower Ca<sup>2+</sup> transient kinetics. NOD mice presented greater number/severity of ventricular arrhythmias both ''in vivo'' and ''in vitro''. In conclusion, NOD mice evoked cardiac electrical and calcium handling disturbances similar to the observed in T1D.
|keywords=Arrhythmias, Electrophysiology. Mitochondria. NOD mice, Type 1 diabetes
|keywords=Arrhythmias, Electrophysiology. Mitochondria. NOD mice, Type 1 diabetes
|editor=[[Plangger M]]
|editor=[[Plangger M]]
|mipnetlab=BR Rio de Janeiro Galina A, BR Rio de Janeiro Institute Biomedical Chemistry
}}
}}
{{Labeling
{{Labeling
|area=Respiration
|area=Respiration
|diseases=Diabetes
|organism=Mouse
|tissues=Heart
|preparations=Isolated mitochondria
|couplingstates=LEAK, OXPHOS
|pathways=N, NS, ROX
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=2020-06
|additional=2020-06
}}
}}

Revision as of 17:43, 4 June 2020

Publications in the MiPMap
Schleier Y, Moreno-Loaiza O, López Alarcón MM, Lopes Martins EG, Braga BC, Ramos IP, Galina A, Medei EH (2020) NOD mice recapitulate the cardiac disturbances observed in type 1 diabetes. J Cardiovasc Transl Res [Epub ahead of print].

» PMID: 32468298

Schleier Y, Moreno-Loaiza O, Lopez Alarcon MM, Lopes Martins EG, Braga BC, Ramos IP, Galina A, Medei EH (2020) J Cardiovasc Transl Res

Abstract: This work aimed at testing the hypothesis that NOD/ShiLtJ mice (NOD) recapitulate the cardiac disturbances observed on type 1 diabetes (T1D). NOD mice were studied 4 weeks after the onset of hyperglycemia, and NOR/Lt mice matched as control. Cardiac function was evaluated by echocardiography and electrocardiography (ECG). Action potentials (AP) and Ca2+ transients were evaluated at whole heart level. Heart mitochondrial function was evaluated by high-resolution respirometry and H2O2 release. NOD mice presented a reduction in hearth weight. Mitochondrial oxygen fluxes and H2O2 release were similar between NOD and NOR mice. ECG revealed a QJ interval prolongation in NOD mice. Furthermore, AP duration at 30% of repolarization was increased, and it depicted slower Ca2+ transient kinetics. NOD mice presented greater number/severity of ventricular arrhythmias both in vivo and in vitro. In conclusion, NOD mice evoked cardiac electrical and calcium handling disturbances similar to the observed in T1D. Keywords: Arrhythmias, Electrophysiology. Mitochondria. NOD mice, Type 1 diabetes Bioblast editor: Plangger M O2k-Network Lab: BR Rio de Janeiro Galina A, BR Rio de Janeiro Institute Biomedical Chemistry


Labels: MiParea: Respiration  Pathology: Diabetes 

Organism: Mouse  Tissue;cell: Heart  Preparation: Isolated mitochondria 


Coupling state: LEAK, OXPHOS  Pathway: N, NS, ROX  HRR: Oxygraph-2k 

2020-06