Effects of PACAP and its fragments in ischemic and oxidative stress-induced cardiomyocyte damage
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1
Department of Biochemistry and Medical Chemistry, University of Pecs, Hungary
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2
Department of Cardiac Surgery , University of Pecs, Hungary
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3
Department of Anatomy , University of Pecs, Hungary
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4
Department of Medical Chemistry, University of Szeged, Hungary
Pituitary adenylate cyclase activating polypeptide (PACAP) has well-known neuroprotective effects, and one of the main factors leading to neuroprotection seems to be its antiapoptotic effects. We have recently shown that PACAP is also cytoprotective in cardiomyocytes. In the present study we summarize the effects of PACAP on survival and signal transduction in cardiomyocytes exposed to oxidative stress or ischemia/reperfusion. Our results show that PACAP increased cell viability by attenuating H2O2- and ischemia/reperfusion-induced apoptosis in a cardiac myocyte culture. PACAP also decreased caspase-3 and -8 activity and increased the expression of the antiapoptotic markers Bcl-2 and Bcl-xL. We showed the involvement of PKA/Bad/14-3-3 and Akt/Bad/14-3-3 signaling pathways in the protective effects exerted by PACAP. Furthermore, we also found that the degree of protection by PACAP was similar to that of ischemic preconditioning, but the two protective strategies together did not cause additive protection. These effects of PACAP were counteracted by the PACAP antagonist PACAP6-38. In summary, our results show that PACAP is able to attenuate oxidative stress- and ischemia/reperfusion-induced cardiomyocyte apoptosis.
Support:OTKA:K72592;F67830;78480
Conference:
12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009.
Presentation Type:
Poster Presentation
Topic:
Pathophysiology and neurology - degenerative disorders
Citation:
Racz
B,
Gasz
B,
Gallyas
F,
Kiss
P,
Horváth
G,
Tamas
A,
Lubics
A,
Toth
G,
Sumegi
B and
Reglődi
D
(2009). Effects of PACAP and its fragments in ischemic and oxidative stress-induced cardiomyocyte damage.
Front. Syst. Neurosci.
Conference Abstract:
12th Meeting of the Hungarian Neuroscience Society.
doi: 10.3389/conf.neuro.01.2009.04.171
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Received:
05 Mar 2009;
Published Online:
05 Mar 2009.
*
Correspondence:
Boglarka Racz, Department of Biochemistry and Medical Chemistry, University of Pecs, Pecs, Hungary, boglarka.racz@aok.pte.hu