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Deoxyribonucleic acid damage/repairproteins are elevated in the failing human myocardium due to idiopathic dilated cardiomyopathy

Jozef Bartunek, MD, PhD^*,*, Marc Vanderheyden, MD, Michiel W. M. Knaapen, PhD, Wouter Tack, RSN^*, Mark M. Kockx, MD, PhD and Marc Goethals, MD^*

^* Cardiovascular Center, Aalst, Belgium
Department of Cardiology, Imelda Ziekenhuis, Bonheiden, Belgium
HistoGeneX, Edegem, Belgium
Department of Pathology, Middelheim Hospital, Antwerp, Belgium

View larger version (89K): [in a new window]   Figure 1 An example of "stringent" TUNEL without the use of proteinase K in positive control (tonsil panel A, x1000) and in a patient with dilated cardiomyopathy (panel B, x200). Arrows indicate the presence of TUNEL-positive nuclei in tonsils. Note that when utilizing the "stringent" approach, no TUNEL-positive labeling has been observed in dilated cardiomyopathy patients.

View larger version (63K): [in a new window]   Figure 2 An example of staining for the deoxyribonucleic acid-protein kinase catalytic subunit (A), proliferative cell nuclear antigen (B), and apurinic/apyrimidine endonuclease/redox factor 1 (C) from a patient with left ventricular ejection fraction 35% (x1000 magnification).

View larger version (12K): [in a new window]   Figure 3 Relationship between the proliferative cell nuclear antigen (PCNA), apurinic/apyrimidine endonuclease/redox factor 1 (APE/Ref-1), and deoxyribonucleic acid-protein kinase catalytic subunit (DNA-PKcs) expression and left ventricular (LV) systolic wall stress.

View larger version (12K): [in a new window]   Figure 4 Relationship between the deoxyribonucleic acid-protein kinase catalytic subunit (DNA-PKcs) and inducible nitric oxide synthase (iNOS) expressions in all patients and in patients with left ventricular ejection fraction (LVEF) 35%.