By Ashkenazi A.
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Extra info for Apo2L/TRAIL
Mitochondria are small and doughnut like. Depletion of sarcomeres and sarcoplasmic reticulae is observed and glycogen is seen to fill the place previously occupied by filaments. These changes result in myocytes that appear to be de-differentiated. Apoptosis has also been identified in biopsies taken from hibernating myocardium at the time of surgical revascularization. ^^ The pathophysiology of hibernation remains under intense investigation. ^^ In long-term hibernation, changes seem to correspond to a genetic program of cellular survival that is induced probably from repetitive episodes of ischemia and reperfusion.
See also chapter 3). Nitric oxide is a molecule with pleiotropic effects on the cardiovascular system. Figure 15. Nitric oxide (NO) is produced when NO synthase (NOS) converts L-arginine to citrulline. The major target of NO in the cardiovascular system is the NO sensitive soluble guanyl cyclase that converts guanosine triphosphate (GTP) to c-GMP. MYOCARDIAL ISCHEMIA 39 NO T Guanyl Cyclase c-AMP Increase C3 Kinases • Other proteins Inliibition Figure 15. Schematic of nitric oxide mediated signaling.
When GTP is bound MYOCARDIAL ISCHEMIA 45 to Ras, activation of the downstream kinases occurs. The cascade includes the MAPKKK (MAP kinase kinase kinase) known as Raf-1, the MAP-KK, known as MEK and the MAPK, known as ERK. Activation of this pathway leads to the phosphorylation of target proteins in both cytosol and nucleus. Such molecules are the p90RSK ribosomal S6 kinase and the transcription factors ELK-1 and CREB. p90RSK is involved in NHE regulation and can also be activated by ERK independent pathways.
Apo2L/TRAIL by Ashkenazi A.