Acute Myocardial Infarction in Humans is Associated with Activation of Programmed Myocyte Cell Death in the Surviving Portion of the Heart

Olivetti, G; Quaini, Federico; Sala, Roberto; Lagrasta, Costanza; Corradi, Domenico; Bonacina, Edgardo; Gambert, Steven; Cigola, Elena; Anversa, Piero

doi:10.1006/jmcc.1996.0193

Cited by 473 publications

(292 citation statements)

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Section: Discussioncontrasting

confidence: 70%

“…10 However, in the present study, much lower rates of apoptosis, ranging from 0.13-0.25%, were detected mainly in the border zone at stages II, and the average prevalence of apoptosis at all stages was 0.13%, as demonstrated by staining with the anti-ss-DNA mAb. The difference in the proportions of cardiomyocyte apoptosis have been reported in the previous studies, 10,[29][30][31] and the difference between the studies might have been due to differences in the tissue samples taken or the method used for analysis of myocardial tissue. 7,32 However, a previous literature by van Empel et al reviewed a prevalence of cardiomyocyte apoptosis ranging from 0.12 to 0.70% in myocardial biopsy specimens obtained from patients with NYHA classes III-IV heart failure, 30,[33][34][35][36][37][38][39][40] which was similar to the figure obtained in the present study.…”

Section: Discussioncontrasting

confidence: 70%

“…Therefore, the variation in the prevalence of cardiomyocyte apoptosis between the reported studies may not have been due to differences in the myocardial tissue samples used for analysis. 10,29 In the present study, the peak SI of cardiomyocytes occured at stage II, when the level of cardiomyocyte necrosis was much higher than that at stage I, indicating that apoptosis and necrosis in cardiomyocytes are responsible for acute cellular loss in the acute stage. 4 As similarly reported in the previous studies, 29,41 cardiomyocyte apoptosis at stage II was noted in the border zone, indicating that apoptosis mediates cell death outside the area of MI.…”

Section: Discussionmentioning

confidence: 42%

“…Furthermore, the rate of cardiomyocyte apoptosis in human MI has been reported to vary (0.12-12%). 9,10 Apoptotic cells are usually identified by terminal deoxynucleotide transferase-mediated dUTP nick end-labeling (TUNEL). Recently, a single-stranded DNA (ss-DNA) monoclonal antibody (clone F7-26) has been reported to be sufficiently sensitive to detect cells at an incipient stage of apoptosis.…”

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confidence: 99%

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Myocardial apoptosis associated with the expression of proinflammatory cytokines during the course of myocardial infarction

et al. 2006

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To clarify the role of myocardial apoptosis associated with the expression of proinflammatory cytokines in human myocardial infarction (MI), we have analyzed the expression of apoptosis positive for single-stranded DNA (ss-DNA) antibody, tumor necrosis factor (TNF)-a, and interleukin (IL)-8 in 147 samples of infarcted myocardial tissue from 65 patients. ss-DNA-positive apoptotic nuclei were found mainly in cardiomyocytes in the border zones and granulation tissue cells in the infarct foci. The ss-DNA index (SI) of cardiomyocytes (average 0.13%) peaked at stage II (established myocardial necrosis), the value being significantly higher than at stages III (macrophage infiltration), IV (granulation formation), and V (scar formation) (Po0.05), whereas the SI of granulation tissue (average 0.08%) at stages III, IV, and V showed no significant differences between the three stages. These results suggest that cardiomyocyte apoptosis in the border zone is responsible for cellular loss in the acute stage of MI, whereas granulation tissue apoptosis may not be involved in the process of ventricular remodeling. TNF-a was expressed in cardiomyocytes in the border zones of infarct foci, but no significant positive correlation was found between SI and TNF-a index in cardiomyocytes (r ¼ 0.08, P ¼ 0.37), suggesting that TNF-a does not serve as a direct trigger of cardiomyocyte apoptosis in vivo. The number of IL-8-positive cells peaked at stage II, and IL-8-myeloperoxidase-double-positive neutrophils were frequently detected, indicating that infiltrating neutrophils are the predominant source of IL-8 in the infarcted myocardium. These results suggest that, in human MI, TNF-a produced by cardiomyocytes does not play a critical role in their apoptosis, and that IL-8 produced by neutrophils is responsible for the subsequent accumulation and activation of neutrophils, thus increasing the degree of myocardial damage.

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Section: Discussioncontrasting

confidence: 70%

Section: Discussioncontrasting

confidence: 70%

Section: Discussionmentioning

confidence: 42%

mentioning

confidence: 99%

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Myocardial apoptosis associated with the expression of proinflammatory cytokines during the course of myocardial infarction

et al. 2006

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“…The loss of cardiomyocytes through apoptosis remains a predominant cause in a variety of cardiovascular diseases. For example, apoptosis has been detected in the animal model of ischemia/reperfusion (Gao et al, 2008), as well as in the patients with acute myocardial infarction (Olivetti et al, 1996), dilated cardiomyopathy (Aharinejad et al, 2008), and metabolic cardiomyopathy (Gürtl et al, 2009). The transgenic mice with tissue specific expression of tumor necrosis factor-α in cardiomyocytes can induce severe pathogenesis of cardiac diseases (Bryant et al, 1998).…”

Section: Mitochondria Mediate Apoptosis In Heartmentioning

confidence: 99%

Mitochondrial network in the heart

Zhou

Gao

et al. 2012

Protein Cell

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Mitochondria are subcellular organelles that provide energy for the cell. They form a dynamic tubular network and play an important role in maintaining the cell function and integrity. Heart is a powerful organ that supplies the motivation for circulation, thereby requiring large amounts of energy. Thus, the healthiness of cardiomyocytes and mitochondria is necessary for the normal cardiac function. Mitochondria not only lie in the center of the cell apoptotic pathway, but also are the major source of reactive oxygen species (ROS) generation. Mitochondrial morphological change includes fission and fusion that are regulated by a large number of proteins. In this review we discuss the regulators of mitochondrial fission/fusion and their association with cell apoptosis, autophagy and ROS production in the heart.

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Pressure related apoptosis in neuronal cell lines

et al. 2000

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Pressure is a crucial component of the cellular environment, and can lead to pathology if it varies beyond its normal range. The increased intra-ocular pressures in acute glaucoma are associated with the loss of neurons by apoptosis. Little is known regarding the interaction between pressure and apoptosis at the level of the cell. The model developed in this study examines the effects of elevated ambient hydrostatic pressure directly upon cultured neuronal lines. Conditions were selected to be within physiological limits: 100 mmHg over and above atmospheric pressure for a period of 2 hr, as seen clinically in acute glaucoma. This system can be used to investigate pressure relatively independently of other variables. Neuronal cell line cultures (B35 and PC12) were subjected to pressure conditions in specially designed pressure chambers. Controls were treated identically, except for the application of pressure, and positive controls were treated with a known apoptotic stimulus. Apoptosis was detected by cell morphology changes and by 2 specific apoptotic markers: TUNEL (Terminal transferase dUTP Nick-End Labeling) and Annexin V. These fluorescent markers were detected and quantified by automated Laser Scanning Cytometry. All techniques showed that increased pressure was associated with a greater level of apoptosis compared to equivalent controls. Our results suggest that pressure alone may act as a stimulus for apoptosis in neuronal cell cultures. This raises the possibility of a more direct relationship at the cellular level between pressure and neuronal loss.

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Acute Myocardial Infarction in Humans is Associated with Activation of Programmed Myocyte Cell Death in the Surviving Portion of the Heart

Cited by 473 publications

References 0 publications

Myocardial apoptosis associated with the expression of proinflammatory cytokines during the course of myocardial infarction

Myocardial apoptosis associated with the expression of proinflammatory cytokines during the course of myocardial infarction

Mitochondrial network in the heart

Pressure related apoptosis in neuronal cell lines

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