Pathologic Assessment of Myocardial Cell Necrosis and Apoptosis after Ischemia and Reperfusion with Molecular and Morphological Markers

Takashi, En; Ashraf, Muhammad

doi:10.1006/jmcc.1999.1067

Cited by 63 publications

(38 citation statements)

References 36 publications

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“…1, B and C). In this study, the border zone accounted for 42.3 Ϯ 5.5% of the area at risk in agreement with a previous study (37). Moreover, this zone was the only one exhibiting the characteristics of an apoptotic area with increases in caspase 3 activity together with TUNEL-positive cardiomyocytes and presence of DNA ladder.…”

Section: Discussionsupporting

confidence: 92%

“…The infarcted (Evans blue and TTC unstained) and border area (Evans blue unstained and TTC stained) represented 56.7 Ϯ 6.2% and 42.3 Ϯ 5.5% of the area at risk, respectively. These values were in agreement with Takashi et al (37).…”

Section: Detection Of Infarcted Border and Perfused Areassupporting

confidence: 93%

“…Sections (50 m) from the six slices were used to measure the different areas as reported in (37,41) (Fig. 1B).…”

Section: Determination Of Infarcted Border and Perfused Areasmentioning

confidence: 99%

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Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone

Monceau¹,

Belikova²,

Kratassiouk³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Monceau, Virginie, Yulia Belikova, Gueorgui Kratassiouk, Estelle Robidel, Françoise Russo-Marie, and Daniele Charlemagne. Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone. Am J Physiol Heart Circ Physiol 291: H965-H971, 2006. First published February 24, 2006 doi:10.1152/ajpheart.01053.2005.-Annexin A5 is a Ca 2ϩ -dependent phospholipid binding protein well known for its high phosphatidylserine affinity. In vitro, translocation to sarcolemma and externalization of endogenous annexin A5 in the cardiomyocyte has recently been demonstrated to exert a proapoptotic effect. To determine whether these in vitro findings occurred in vivo, we performed myocardial infarction (MI) and studied the time course of apoptosis and annexin A5 localization (0.5 to 8 h) in the border zone around the infarcted area. This zone that was defined as Evans blue unstained and triphenyltetrazolium chloride (TTC) stained, represented 42.3 Ϯ 5.5% of the area at risk and showed apoptotic characteristics (significant increases in caspase 3 activity 2.3-fold at 0.5 h; P Ͻ 0.05), transferase-mediated dUTP nick-end labelingpositive cardiomyocytes (15.8 Ϯ 0.8% at 8 h), and DNA ladder. When compared with sham-operated rats, we found that in this area, annexin A5 was translocated to the sarcolemma as early as 0.5 h after MI and that translocation increased with time. Moreover, the amount of annexin A5 was unchanged in the border zone and decreased in the infarcted area after 1 h (77.1 Ϯ 4.8%; P Ͻ 0.01 vs. perfused area), suggesting a release in the latter but not in the former. In conclusion, we demonstrated that annexin A5 translocation is an early and rapid event of the whole border zone, likely due to Ca 2ϩ increase. Part of this translocation occurred in areas where apoptosis was later detected and suggests that in vivo as in vitro annexin A5 might be involved in the regulation of early apoptotic events during cardiac pathological situations. myocardial ischemia; terminal deoxyribonucleotide transferase ANNEXINS are a structurally related family of proteins known to bind phospholipids in a Ca 2ϩ

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Section: Discussionsupporting

confidence: 92%

Section: Detection Of Infarcted Border and Perfused Areassupporting

confidence: 93%

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Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone

Monceau¹,

Belikova²,

Kratassiouk³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…33 We were unable to determine the influence of microscopic necrosis on the relationship between myocardial energetic status and deformation parameters in the early stages of acute ischemia (40 minutes), because subendocardial necrosis was indicated by TTC in only 1 animal, and the presence of microscopic necrosis was conceivable. However, to evaluate the association of necrosis and energetic or strain parameters was not the primary aim of our study and has been discussed elsewhere.…”

Section: Limitationsmentioning

confidence: 97%

Doppler Strain Imaging Closely Reflects Myocardial Energetic Status in Acute Progressive Ischemia and Indicates Energetic Recovery After Reperfusion

Kořínek

Sengupta

Wang

et al. 2008

Journal of the American Society of Echocardiography

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“…The macrophages do not release proinflammatory cytokines but rather secrete anti-inflammatory cytokines (e.g., TGF-beta and IL-10) [36]. The selective anti-inflammatory functional phenotype prevents the infiltration of inflammatory cells [35][36][37][38].…”

Section: Ultrastructural Features In Apoptosismentioning

confidence: 98%

Ultrastructural definition of apoptosis in heart failure

2008

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Cardiac myocytes die through apoptosis, oncosis, and autophagy. Apoptosis affects single cells and is morphologically characterized by nuclear fragmentation with generation of apoptotic bodies that can be seen either within dying cells or free in the interstitial spaces. Dead myocytes are removed by macrophages through phagocytosis without triggering inflammation. The circulating markers of myocyte necrosis are not increased by apoptosis. The morphologic changes of the induction and early execution phases are seen at electron microscopy while late fragmentation is visible on both light and electron microscopy. Immunoelectron microscopy provides combined functional and structural information showing cytochrome c immuno-labelling release from mitochondria, TUNEL labelling of apoptotic nuclei, annexin V translocation in the outer plasma cell layer. Oncosis is characterized by specific morphologic features that may coexist with apoptosis, especially in ischemic myocardium. Autophagy is a defense process that is associated with significant myocardial damage and necrosis when removal of the lysosomal content is impaired. Morphological features of apoptosis, oncosis, and autophagocytosis may coexist at the same time. Although dead myocytes showing characteristics of autophagy and apoptosis are rarely observed in human decompensated hearts, autophagic vacuoles, and early apoptotic changes may be seen more often in morphologically viable myocytes. Such features may occur in failing hearts of both ischemic and non-ischemic etiology. The shared mode of cardiac myocyte death in failing human hearts of different etiologies suggests that preservation of myocyte integrity may be possible by similar therapeutic strategies.

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Pathologic Assessment of Myocardial Cell Necrosis and Apoptosis after Ischemia and Reperfusion with Molecular and Morphological Markers

Cited by 63 publications

References 36 publications

Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone

Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone

Doppler Strain Imaging Closely Reflects Myocardial Energetic Status in Acute Progressive Ischemia and Indicates Energetic Recovery After Reperfusion

Ultrastructural definition of apoptosis in heart failure

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