Aging aggravates heterogeneities in cell-size and stress-intolerance of cardiac ventricular myocytes

Dyachenko, V. V.; Rueckschloss, Uwe; Isenberg, Gerrit

doi:10.1016/j.exger.2006.03.003

Cited by 5 publications

(6 citation statements)

References 19 publications

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“…Cells used in this study exhibited the agerelated increase in cell size reported previously in ventricular myocytes from rat, mouse, and sheep hearts (7,8,11,16,29). We also found that the amplitudes of contractions, expressed as a percentage of diastolic cell length, were similar in young adult and aged cells under control conditions.…”

Section: Discussionsupporting

confidence: 83%

“…11,29), is that the yield of viable myocytes is somewhat lower from aged hearts than from younger hearts. However, cells investigated in the present study had morphological and physiological characteristics similar to those previously described in aged ventricular myocytes (7,8,11,16,20,29). Thus the cells utilized in this investigation are similar to those investigated in previous studies of the aging cardiac myocyte.…”

Section: Discussionsupporting

confidence: 76%

“…Cell width was not affected by age, but cell area was significantly greater in myocytes isolated from aged hearts compared with cells from younger hearts ( Table 1). This characteristic age-related increase in cell size has been described previously in ventricular myocytes isolated from aged rat, mouse, and sheep hearts (7,8,11,16,29). To compensate for differences in cell size, all contraction data were normalized either to cell length or to control values before ischemia.…”

Section: Resultsmentioning

confidence: 83%

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Effects of ischemia and reperfusion on isolated ventricular myocytes from young adult and aged Fischer 344 rat hearts

O'Brien¹,

Ferguson²,

Howlett³

2008

American Journal of Physiology-Heart and Circulatory Physiology

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This study examined the impact of age on contractile function, Ca(2+) homeostasis, and cell viability in isolated myocytes exposed to simulated ischemia and reperfusion. Ventricular myocytes were isolated from anesthetized young adult (3 mo) and aged (24 mo) male Fischer 344 rats. Cells were field-stimulated at 4 Hz (37 degrees C), exposed to simulated ischemia, and reperfused with Tyrode solution. Cell shortening and intracellular Ca(2+) were measured simultaneously with an edge detector and fura-2. Cell viability was assessed by Trypan blue exclusion. Ischemia (20-45 min) depressed amplitudes of contraction equally in isolated myocytes from young adult and aged animals. The degree of postischemic contractile depression (stunning) was comparable in both groups. Ca(2+) transient amplitudes were depressed in early reperfusion in young adult and aged cells and then recovered to preischemic levels in both groups. Cell viability also declined equally in reperfusion in both groups. In short, some cellular responses to simulated ischemia and reperfusion were similar in both groups. Even so, aged myocytes exhibited a much greater and more prolonged accumulation of diastolic Ca(2+) in ischemia and in early reperfusion compared with myocytes from younger animals. In addition, the degree of mechanical alternans in ischemia increased significantly with age. The observation that there is an age-related increase in accumulation of diastolic Ca(2+) in ischemia and early reperfusion may account for the increased sensitivity to ischemia and reperfusion injury in the aging heart. The occurrence of mechanical alternans in ischemia may contribute to contractile dysfunction in ischemia in the aging heart.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionsupporting

confidence: 76%

Section: Resultsmentioning

confidence: 83%

See 1 more Smart Citation

Effects of ischemia and reperfusion on isolated ventricular myocytes from young adult and aged Fischer 344 rat hearts

O'Brien¹,

Ferguson²,

Howlett³

2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…Cytochrome c release from mitochondria is a key step leading to programmed cell death, and, indeed, the rate of programmed cell death in the left ventricle increases with age and contributes to a reduction in cardiomyocyte number and an increase in the extent of fibrosis (for a review, see Higami and Shimokawa, 2000;Bernecker et al, 2003). Aging also aggravates the heterogeneities in cardiomyocyte size (Dyachenko et al, 2006). Finally, apart from the increased oxidative stress, mitochondria from aged hearts display reduced membrane potential (Savitha and Panneerselvam, 2006;Serviddio et al, 2007), which may contribute to reduced ATP synthesis (for reviews, see Pepe, 2000;Di Lisa and Bernardi, 2005).…”

Section: E Aging and Cardioprotectionmentioning

confidence: 99%

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

Ferdinándy¹,

Schulz²,

Baxter³

2007

Pharmacol Rev

648

615

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“…The data presented here showed that exercise increased mitochondrial Δψ and ATP synthase activity in older mice, but did not affected ROS production. Hearts of old mice contain a subpopulation of myocytes with reduced mitochondrial stress-tolerance that is attributed to an age-dependent reduction of cellular ROS defence capacity [47]. Our data suggest that, to a certain extent, endurance exercise can attenuate age-related changes in cardiac mitochondria, thus to maintain their capacity to produce ATP.…”

Section: Discussionmentioning

confidence: 68%

Physical Exercise Regulates p53 Activity Targeting SCO2 and Increases Mitochondrial COX Biogenesis in Cardiac Muscle with Age

et al. 2011

PLoS ONE

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The purpose of this study was to outline the timelines of mitochondrial function, oxidative stress and cytochrome c oxidase complex (COX) biogenesis in cardiac muscle with age, and to evaluate whether and how these age-related changes were attenuated by exercise. ICR/CD-1 mice were treated with pifithrin-μ (PFTμ), sacrificed and studied at different ages; ICR/CD-1 mice at younger or older ages were randomized to endurance treadmill running and sedentary conditions. The results showed that mRNA expression of p53 and its protein levels in mitochondria increased with age in cardiac muscle, accompanied by increased mitochondrial oxidative stress, reduced expression of COX subunits and assembly proteins, and decreased expression of most markers in mitochondrial biogenesis. Most of these age-related changes including p53 activity targeting cytochrome oxidase deficient homolog 2 (SCO2), p53 translocation to mitochondria and COX biogenesis were attenuated by exercise in older mice. PFTμ, an inhibitor blocking p53 translocation to mitochondria, increased COX biogenesis in older mice, but not in young mice. Our data suggest that physical exercise attenuates age-related changes in mitochondrial COX biogenesis and p53 activity targeting SCO2 and mitochondria, and thereby induces antisenescent and protective effects in cardiac muscle.

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Aging aggravates heterogeneities in cell-size and stress-intolerance of cardiac ventricular myocytes

Cited by 5 publications

References 19 publications

Effects of ischemia and reperfusion on isolated ventricular myocytes from young adult and aged Fischer 344 rat hearts

Effects of ischemia and reperfusion on isolated ventricular myocytes from young adult and aged Fischer 344 rat hearts

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

Physical Exercise Regulates p53 Activity Targeting SCO2 and Increases Mitochondrial COX Biogenesis in Cardiac Muscle with Age

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