Warm blood cardioplegic arrest induces mitochondrial-mediated cardiomyocyte apoptosis associated with increased urocortin expression in viable cells

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Presentation transcript:

Warm blood cardioplegic arrest induces mitochondrial-mediated cardiomyocyte apoptosis associated with increased urocortin expression in viable cells Tiziano M. Scarabelli, MD, PhD, Evasio Pasini, MD, Gianna Ferrari, MD, Mario Ferrari, MD, Anastasis Stephanou, PhD, Kevin Lawrence, PhD, Paul Townsend, PhD, Carol Chen-Scarabelli, MSc, Gianluca Gitti, BSc, Louis Saravolatz, MD, David Latchman, PhD, DSc, Richard A. Knight, MD, PhD, Julius M. Gardin, MD The Journal of Thoracic and Cardiovascular Surgery Volume 128, Issue 3, Pages 364-371 (September 2004) DOI: 10.1016/j.jtcvs.2003.11.028

Figure 1 A, Control precardioplegic heart (group A) exhibiting no TUNEL-positive staining or processing of caspase-3. Orange nuclei are stained with propidium iodide. B, Control precardioplegic heart (group B) showing no processing of caspase-8 or caspase-9. Cells are counterstained with propidium iodide. C, Postcardioplegic heart (group A): yellow TUNEL-positive nuclei colocalize with cytoplasmic anti-active caspase-3–positive labeling (bright red). D, Postcardioplegic heart (group B): cardiac myocytes showing colocalization between TUNEL-positive (yellow/green nuclei) and cytoplasmic anti-active caspase-3–positive staining (bright red). (Original magnifications: A, B, and C, 400×; D, 650×.) The Journal of Thoracic and Cardiovascular Surgery 2004 128, 364-371DOI: (10.1016/j.jtcvs.2003.11.028)

Figure 2 Processing of caspase-3 (C3), caspase-8 (C8), and caspase-9 (C9) in precardioplegic (pre-CP) and postcardioplegic (post-CP) samples from groups A and B analyzed by means of Western blotting. The housekeeping gene actin was used as a protein-loading control. The Journal of Thoracic and Cardiovascular Surgery 2004 128, 364-371DOI: (10.1016/j.jtcvs.2003.11.028)

Figure 3 Serial myocardial sections from a postcardioplegic heart (group B) showing activation of caspase-9 (B, bright red) and caspase-8 (C, bright green) in cardiac myocytes, as identified by an anti-desmin red banding running perpendicularly to the cell bodies (A). (Original magnification 400×.) The Journal of Thoracic and Cardiovascular Surgery 2004 128, 364-371DOI: (10.1016/j.jtcvs.2003.11.028)

Figure 4 Basal expression of urocortin in cardiac myocytes from a control heart (group A). No TUNEL-positive cells are detected (B). Postcardioplegic heart (group B): cardiac myocytes exhibiting cytosolic urocortin-positive staining (bright red) are consistently TUNEL negative. TUNEL-positive nuclei appear yellow (D). Cardiac myocytes are recognizable by the anti-desmin red banding running perpendicularly to their cellular body (A and C). (Original magnification 400×.) The Journal of Thoracic and Cardiovascular Surgery 2004 128, 364-371DOI: (10.1016/j.jtcvs.2003.11.028)

Figure 5 Serial atrial sections from a postcardioplegic heart (group B). Induction of urocortin in cardiac myocytes (B, bright red cytosolic staining) is associated with TUNEL negativity (A, TUNEL-positive nuclei appear yellow) and overexpression of the Kir6.1 potassium channel (bright green cytosolic staining), which is detected not only in urocortin-positive cells but also in urocortin-negative neighboring cells (C). Cardiac myocytes are labeled by an anti-desmin antibody (A). (Original magnification 400×.) The Journal of Thoracic and Cardiovascular Surgery 2004 128, 364-371DOI: (10.1016/j.jtcvs.2003.11.028)