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国际生理学与病理学期刊
SJR: 0.116

ISSN 打印: 2155-014X
ISSN 在线: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

国际生理学与病理学期刊

DOI: 10.1615/IntJPhysPathophys.v1.i3.60
pages 245-258

Changes in UCP2 and UCP3 Genes Expression, in Heart Function and Oxygen Cost of Myocardial Work under Aging and Ischemia-Reperfusion

Yulia V. Goshovska
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv
Olexandr O. Lisovyi
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv
Tetyana V Shimanskaya
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv
Vadim F. Sagach
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine

ABSTRACT

To examine effects of ischemia-reperfusion on UCP's genes expression, heart function and oxygen cost of myocardial work hearts of adult (6 mo) and old (24 mo) rats were perfused by Langendorf preparation and subjected to 20 min ischemia and 40 min of reperfusion. Mitochondrial permeability transition due to ischemic stimuli was evaluated by release of mitochondrial factor (λ = 250 nm) which was previously shown as a marker of MPTP opening. Expression of UCPs was detected by reverse transcriptional polymerase chain reaction. Mitochondrial membrane potential (Δψm) and oxygen consumption in isolated heart mitochondria of adult and old rats were measured. It was shown that impaired function of aging rat hearts was accompanied with increased oxygen cost of myocardial work and lower mitochondrial membrane potential comparing with adult rats. At the same time no mitochondrial factor was detected in initial state. Reperfusional disturbances of cardiodynamic, contractile activity of myocardium and noneffective oxygen utilization in early period of reperfusion were less intensive in aged hearts than in adult ones. However, it was detected greater amount of mitochondrial factor in outflow solution in reperfused aged heart indicating excessive MPTP opening. Levels of mRNA of UCP2 in aging hearts were higher and mRNA levels of UCP3 were tended to increase. Expression of UCP2 and UCP3 in adult myocardium was stimulated by ischemia- reperfusion, whereas there was no such effect in aging hearts. It is concluded that MPTP and uncoupling proteins are implicated in age-depended heart dysfunction and pathological mechanisms developed during ischemia-reperfusion.


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