http://www.cnr.it/ontology/cnr/individuo/prodotto/ID186496
Time course and distribution of TUNEL nuclear positivity of cardiomyocytes in a chronic rat model of coronary occlusion with and without reperfusion (Abstract/Poster in rivista)
- Type
- Label
- Time course and distribution of TUNEL nuclear positivity of cardiomyocytes in a chronic rat model of coronary occlusion with and without reperfusion (Abstract/Poster in rivista) (literal)
- Anno
- 2010-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1093/cvr/cvq174 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- G. Pelosi ; M.Matteucci ; C. Kusmic ; N. Vesentini ; F. Piccolomini ; F. Viglione ; MG. Trivella ;
A. L'Abbate (literal)
- Pagina inizio
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
- Note
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Istituto di Fisiologia Clinica C.N.R. Pisa
SSSA Pisa (literal)
- Titolo
- Time course and distribution of TUNEL nuclear positivity of cardiomyocytes in a chronic rat model of coronary occlusion with and without reperfusion (literal)
- Abstract
- Occlusion of a coronary artery either permanent or followed by reperfusion is known to cause irreversible
myocellular death mainly by \"oncotic\" modality. DNA fragmentation by in situ terminal
deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) has been frequently
detected at light microscopy (LM) in oncotic cells and believed to be an index of a caspase-mediated
\"apoptotic\" type of cellular death, although typical apoptotic ultrastructural features have never
been observed. The contribution of this DNA fragmentation- associated oncotic myocellular
death to overall irreversible myocardial necrosis after ischemia and ischemia reperfusion is still
questionable and its time course unknown.
Purpose: To assess the time course and distribution of TUNEL nuclear positivity of cardiomyocytes
within the infarcted and ischemic-reperfused myocardium of rat heart over a 3 day time span.
Methods: Male rats underwent permanent (I, n ¼ 12) or transient (I-R, 30min occlusion followed
by reperfusion, n ¼ 12) ligation of the left anterior descending coronary artery and hearts explanted
at 1h (groups 1h I, 1h I-R), 1 day (groups 1d I, 1d I-R) and 3 days (groups 3d I and 3d I-R).
Sham-operated animals served as controls (C, n ¼ 6). Histology (H&E and Masson trichromic
stain) and TUNEL assay were performed on 10 consecutive serial slices at two levels distal to
the ligature for LM morphometric assessment of necrosis and nuclear TUNEL analysis.
Results: In groups 1h I and 1h I-R neither cellular necrosis or TUNEL positivity could be detected
both in risk and control areas as well as in C hearts. In group 1d I contraction bands in the periphery
and coagulation necrotic myocells in the central part of infarction showed 30 + 5% and 45 + 3%
of TUNEL positive nuclei respectively. In group 1d I-R 50 + 5% of contraction band necrotic cells
had TUNEL positive nuclei. In groups 3d I and 3d I-R most of the still visible nuclei of necrotic myocytes
were positive (94 + 5 and 95 + 4% respectively). TUNEL positivity was never observed in
myocytes without LM evidence of cellular necrosis.
Conclusion: The present findings demonstrate that DNA fragmentation: a) invariably coexists with
myocellular necrosis prior to complete nuclear demise over a 3 day time span, b) it has a comparable
incidence in I and I-R groups, c) it persists at 3 days with an even higher incidence. The possibility
that TUNEL positivity could identify a specific caspase-dependent subpopulation of irreversibly
damaged cardiomyocytes within the context of ischemic and ischemic-reperfusion necrosis is
suggested. (literal)
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