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Turan 2018 MiP2018
Diseases Aging;senescence  +
Has abstract [[Image:MITOEAGLE-logo.jpg|left|100px|link
[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]] Cardiovascular diseases, including depressed cardiac function in aged-individiuals, remain a major public health problem in all over the world. From an epidemiologic perspective, attenuation of cardiovascular disease-incidence and severity has been interested largely since very long time. Clinical and experimental studies point out the main contribution of mitochondrial-derived reactive oxygen species, ROS, as an important candidate for aged-associated cardiac dysfunction. Here we aimed to determine whether a mitochondria-targeted antioxidant, MitoTEMPO, could preserve the cardiovascular dysfunction in aged-rats ''in vitro''. We used freshly isolated ventricular cardiomyocytes from male 24-month old rats comparison to those of 6-month old rats. Patch-clamp examinations showed that the prolonged action potential was preversed with mitoTEMPO, significantly, due to normalization of the depressed voltage-dependent K<sup>+</sup>-channel currents. The mitoTEMPO application also significantly attenuated the activated ATP-sensitive K<sup>+</sup>-currents and Na<sup>+</sup>/K<sup>+</sup>-pump currents. Furthermore, the fluorescence analysis of confocal images exhibited that the intracellular levels of both free Zn<sup>2+</sup> and Ca<sup>2+</sup> were markedly normalized with MitoTEMPO treatment in cardiomyocytes from aged-rats. The markedly increased ROS level in aged-cardiomyocytes and depolarized mitochondrial membrane potential could be preversed with mitoTEMPO, as well. MitoTEMPO also maintained the intracellular pH level in these senescent cells. Biochemical analysis presented that the protein expression level of some Zn<sup>2+</sup>-transporters localized to both sarcoplasmic reticulum and mictochondria and responsible of both influx of Zn<sup>2+</sup> into cytosol and cytosolic Zn<sup>2+</sup>-efflux was found to be altered, due to alterations in protein expression levels of some Zn<sup>2+</sup>-transporters, localized to sarcolemma and these suborgannels in cardiomyocytes from ager-rat heart. Overall, our present data from aged-rats demonstrated that not only mitochondria but also sarcoplasmic reticulum and the associted intracellular homeostasis of free Zn<sup>2+</sup>, at most, via alteration in Zn<sup>2+</sup>-transporters seem to be good candidates as cardioprotective/cardiotherapeutic actors in cardiomyocytes against aging-associated alterations in mammalian myocardium.
iated alterations in mammalian myocardium.  +
Has editor [[Kandolf G]]  + , [[Plangger M]]  +
Has title [[Image:MiPsocietyLOGO.JPG|left|90px|Mitochondrial Physiology Society|MiPsociety]] Role of mitochondria-associated oxidative stress in aging heart function.  +
Mammal and model Rat  +
MiP area Pharmacology;toxicology  + , mt-Medicine  +
Respiration and regulation Ion;substrate transport  +
Stress Oxidative stress;RONS  +
Was submitted in year 2018  +
Was submitted to event MiP2018/MitoEAGLE Jurmala LV +
Was written by Turan B +
Categories Abstracts
Modification date
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07:44:09, 20 August 2018  +
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