Mitochondrial Energy-producing Ability Research Articles

Comparison of transplantation effects of cardiac progenitor cell types on the mitochondrial energy-producing ability after myocardial infarction in rats

Comparison of transplantation effects of cardiac progenitor cell types on the mitochondrial energy-producing ability after myocardial infarction in rats

Comparison of transplantation effects of cardiac progenitor cell types on the mitochondrial energy-producing ability after myocardial infarction in rats

Comparison of transplantation effects of cardiac progenitor cell types on the mitochondrial energy-producing ability after myocardial infarction in rats

Comparison of transplantation effects among cardiac progenitor cell types on the mitochondrial energy-producing ability after myocardial infarction in rats

Comparison of transplantation effects among cardiac progenitor cell types on the mitochondrial energy-producing ability after myocardial infarction in rats

Effects of cardiosphere-derived cell transplantation on cardiac mitochondrial oxygen consumption after myocardial infarction in rats.

It is postulated that impaired mitochondrial energy-producing ability may lead to the development of chronic heart failure following an acute myocardial infarction. In this study, the effects of transplantation of cardiosphere-derived cells (CDCs) into the viable cardiac tissue after a myocardial infarction on the cardiac mitochondrial oxygen consumption rate (OCR) were examined. CDCs isolated from adult rat cardiac tissue fragments were cultured. Myocardial infarction was induced by ligation of the left ventricular coronary artery in rats. Immediately after coronary artery ligation (CAL), approximately 1 million CDCs were injected into the viable myocardium around the infarct area. Eight weeks after CAL, animals without transplantation showed signs of heart failure such as impaired cardiac pump function. Furthermore, the mitochondrial OCR of the viable cardiac tissue in rats with heart failure was reduced. In contrast, the cardiac pump function and mitochondrial OCR were preserved without a reduction in the infarct size in the animals with transplantation of CDCs. These results suggest that the transplantation of CDCs into the infarcted rat heart contributes to a preservation of mitochondrial function, leading to an improvement of cardiac contractile function without regeneration of cardiac tissues.

Effects of cardiac c-Kit- or Sca-1-positive cells transplantation on the mitochondrial energy-producing ability after myocardial infarction in rats

Effects of cardiac c-Kit- or Sca-1-positive cells transplantation on the mitochondrial energy-producing ability after myocardial infarction in rats

Effects of 2-Octynyladenosine (YT-146) on Mitochondrial Function in Ischemic/Reperfused Rat Hearts.

This study investigated the effects of an adenosine receptor agonist, 2-octynyladenosine (YT-146), on mitochondrial function in ischemic and ischemic/reperfused hearts. Isolated rat hearts were perfused in the Langendorff manner with a constant flow rate, and exposed to 30 min of ischemia followed by 60 min of reperfusion. Preischemic treatment with YT-146 significantly improved postischemic recovery of left ventricular developed pressure. The high-energy phosphate content in reperfused hearts treated with YT-146 was also more greatly restored than in untreated hearts. YT-146 treatment attenuated the Na(+) content of a mitochondria-enriched fraction, but not the myocardial Na(+) content, at the end of ischemia. These results suggest that preischemic YT-146 treatment preserves the energy-producing ability of mitochondria during ischemia in the Na(+)-accumulated myocardium. YT-146 also attenuated both the sodium lactate-induced decrease in mitochondrial energy-producing ability and the increase in mitochondrial Na(+) concentration in the myocardial skinned fibers. YT-146 may attenuate Na(+) influx to myocardial mitochondria in ischemic cardiac cells, resulting in both preservation of the ability of mitochondria to produce energy and enhancement of the contractile recovery in reperfused hearts. Our findings suggest that the cardioprotective effects of YT-146 against ischemia/reperfusion injury are at least partially due to the preservation of mitochondrial function in the ischemic myocardium.

Protective effect of geranylgeranylacetone via enhanced induction of HSPB1 and HSPB8 in mitochondria of the failing heart following myocardial infarction in rats

The mechanisms underlying mitochondrial impairment in the failing heart are not yet clear. In a previous study, we found that the levels of small heat shock proteins (HSP) such as mitochondrial HSPB1 and HSPB8 in the failing heart following myocardial infarction were decreased. In the present study, to verify the hypothesis that mitochondrial dysfunction in the failing heart is associated with alterations in mitochondrial small heat shock proteins, we examined the effects of geranylgeranylacetone, a heat shock protein inducer, on the cardiac mitochondrial function after myocardial infarction. When hemodynamic parameters of rats with myocardial infarction were measured at the 8th (8W) week after coronary artery ligation (CAL), the 8W-CAL showed signs of chronic heart failure concomitant with a reduced mitochondrial oxygen consumption rate. HSPB1 and HSPB8 contents in the mitochondrial fraction prepared from the failing heart were decreased, suggesting that an attenuation of mitochondrial translocation of HSPB1 and HSPB8 had led to an impairment of mitochondrial energy-producing ability. Geranylgeranylacetone treatment from the 2nd to 8th week after myocardial infarction attenuated the reduction in mitochondrial HSPB1 and HSPB8 contents. Furthermore, the mitochondrial energy-producing ability and cardiac pump function were preserved by orally administered geranylgeranylacetone during the development of heart failure. These results suggest that the induction of small heat shock proteins in the infarcted heart by geranylgeranylacetone treatment contributed to the preservation of mitochondrial function, leading to an improvement of cardiac contractile function.

Changes in Small Heat Shock Proteins HSPB1, HSPB5 and HSPB8 in Mitochondria of the Failing Heart Following Myocardial Infarction in Rats

The mechanisms underlying mitochondrial impairment in the failing heart are not yet clearly defined. In the present study, we examined the involvement of changes in small heat shock proteins (HSPs) such as HSPB1, HSPB5 and HSPB8 in mitochondrial dysfunction of the failing heart. Hemodynamic parameters of rats with myocardial infarction at the 2nd and 8th weeks (2W- and 8W-) after coronary artery ligation (CAL) were measured. The 8W-CAL rats, but not the 2W-CAL ones, showed the signs of the chronic heart failure concomitant with a reduced mitochondrial oxygen consumption rate. In the mitochondrial fraction prepared from the heart of the 2W-CAL animals, the contents of small HSPs and phosphorylated small HSPs were increased, suggesting that these increases contributed to the preservation of the mitochondrial energy-producing ability. In the failing heart, HSPB1 and HSPB8 contents and phosphorylated small HSP contents in the mitochondrial fraction were decreased, suggesting that a reduction in mitochondrial translocation of these small HSPs led to impaired mitochondrial energy-producing ability. To further define the submitochondrial locations of these small HSPs, we performed mitochondrial subfractionation. The contents of small HSPs in the 2W-CAL rats were increased in the mitochondrial inner-membrane fraction, whereas those of the 8W-CAL rats were reversed to those of the control animals. These findings suggest that small HSPs, at least in part, play an important role in the development of the impaired mitochondrial energy-producing ability that leads to heart failure after a myocardial infarction.

Ultrastructural evidence of mitochondrial abnormalities in postresuscitation myocardial dysfunction

ObjectivesThough there is evidence to implicate that the mitochondrion may play an important role in the development of postresuscitation myocardial dysfunction, limited data are available regarding the ultrastructural alterations of the mitochondria, mitochondrial energy-producing ability, and their relationship to postresuscitation myocardial dysfunction. This study was designed to determine whether mitochondrial abnormalities contribute to the development of postresuscitation myocardial dysfunction. MethodsFifteen anesthetized male Sprague-Dawley rats were randomized to: (1) global myocardial ischemia/reperfusion, in which 8min of ventricular fibrillation was induced and successful defibrillation was achieved after 6min of cardiopulmonary resuscitation (CPR); (2) global myocardial ischemia, in which ventricular fibrillation and CPR were performed without defibrillation attempt; and (3) sham control. ResultsMyocardial function was significantly impaired after resuscitation. Mitochondria were massively swollen in global ischemic hearts and mildly swollen in the resuscitated hearts. Concomitantly, ATP levels abruptly declined during global ischemia and partially recovered after resuscitation. Furthermore, mitochondrial abnormalities were supported by the incapability of utilizing energy substrates manifested by the accumulations of intramyocellular lipid droplets and glycogen deposits. ConclusionsIn this model of cardiac arrest and CPR, the presence of ultrastructural mitochondrial abnormalities, further evidenced by the incapability of utilizing energy substrates and impairment of energy-production, might, in part, contribute to the development of postresuscitation myocardial dysfunction.

Possible Involvement of Mitochondrial Energy-Producing Ability in the Development of Right Ventricular Failure in Monocrotaline-Induced Pulmonary Hypertensive Rats

The present study was undertaken to explore the possible involvement of alterations in the mitochondrial energy-producing ability in the development of the right ventricular failure in monocrotaline-administered rats. The rats at the 6th week after subcutaneous injection of 60 mg/kg monocrotaline revealed marked myocardial hypertrophy and fibrosis, that is, severe cardiac remodeling. The time-course study on the cardiac hemodynamics of the monocrotaline-administered rat by the cannula and echocardiographic methods showed a reduction in cardiac double product, a decrease in cardiac output index, and an increase in the right ventricular Tei index, suggesting that the right ventricular failure was induced at the 6th week after monocrotaline administration in rats. The mitochondrial oxygen consumption rate of the right ventricular muscle isolated from the monocrotaline-administered animal was decreased, which was associated with a reduction in myocardial high-energy phosphates. Furthermore, the decrease in mitochondrial oxygen consumption rate was inversely related to the increase in the right ventricular Tei index of the monocrotaline-administered rats. These results suggest that impairment of the mitochondrial energy-producing ability is involved in the development of the right ventricular failure in monocrotaline-induced pulmonary hypertensive rats.

Changes in mitochondrial energy-producing ability in the right ventricular muscle of monocrotaline-induced pulmonary hypertensive rats

Changes in mitochondrial energy-producing ability in the right ventricular muscle of monocrotaline-induced pulmonary hypertensive rats