Preconditioning decreases Bax expression, PMN accumulation and apoptosis in reperfused rat heart

doi:10.1016/S0008-6363(99)00393-4

Cardiovascular Research 2000 45(3):661-670; doi:10.1016/S0008-6363(99)00393-4
© 2000 by European Society of Cardiology

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Preconditioning decreases Bax expression, PMN accumulation and apoptosis in reperfused rat heart

Masanori Nakamura^a, Ning-Ping Wang^a, Zhi-Qing Zhao^a, Josiah N Wilcox^b, Vinod Thourani^a, Robert A Guyton^a and Jakob Vinten-Johansen^a^,*

^aDepartment of Cardiothoracic Surgery, Emory University School of Medicine, Atlanta, GA 30365-2225, USA
^bDepartment of Hematology/Oncology, Emory University School of Medicine, Atlanta, GA 30365-2225, USA

^* Corresponding author. Tel.: +1-404-686-2511; fax: +1-404-686-4888 jvinten{at}emory.edu

Objective: Recent studies suggest that ischemic preconditioning(IPC) inhibits myocardial apoptosis after ischemia and reperfusion.This study tested the hypothesis that IPC reduces ischemia/reperfusion-inducedmyocardial apoptosis by inhibiting neutrophil (PMN) accumulationand altering expression of Bcl-2 and Bax proteins. Methods:Eighteen rats were subjected to 30 min of left coronary arteryocclusion followed by 180 min of reperfusion with IPC (5 minischemia and 10 min of reperfusion, n=10) or without IPC (n=8).Myocardial apoptosis was detected histologically using the terminaltransferase UTP nick end labeling (TUNEL) assay and confirmedby DNA ladder on agarose gel electrophoresis. PMN accumulationwas detected immunohistochemically with anti-rat CD18 antibody(WT3) and expression of Bcl-2 and Bax proteins was analyzedusing Western blot assay. Results: IPC significantly decreasedTUNEL positive cells (% total nuclei) in the ischemic zone from28.6±2.8 to 3.4± 0.9 (P<0.05), consistent withthe absence of DNA ladders in the IPC group. IPC significantlyattenuated PMN accumulation (cells/mm² myocardium) in the ischemiczone from 243±19 to 118±19 (P<0.05). By regressionanalysis, there was a significant correlation between TUNELpositive cells and accumulated CD18 positive PMNs in the ischemiczone (r=0.8, P<0.001), which was shifted downward by IPC.Densitometrically, IPC significantly attenuated the ischemia/reperfusion-upregulatedexpression of Bax protein in the ischemic zone from 204±57%in the control group to 76±7% (P<0.05), while theexpression of Bcl-2 was not different from the non-ischemiczone in either group. Conclusion: These data suggest that ischemicpreconditioning may reduce myocardial apoptosis by inhibitingPMN accumulation and down-regulating expression of Bax.

KEYWORDS Apoptosis; Ischemia; Leukocytes; Preconditioning; Reperfusion

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