Abstract
266 Apoptotic pathways may influence rejection of allografts, but the significance of individual components in these pathways has yet to be determined. This study was designed to evaluate the role of bcl-2 in preventing allograft rejection in the mouse. A transgenic mouse was established in this lab in which the BCL-2 protooncogene is expressed under the control of the H2K promoter. High levels of bcl-2 were detected in cardiac tissue by Western blot analysis. Hearts from neonates of this founderline and their littermate controls were used in a model of cardiac transplantation across major histocompatibility barriers (H2b--> H2d). Briefly, the heart of a neonatal C57B1/Ka mouse is removed and placed in the subcutaneous tissue of the ear of an adult BALB/c mouse. Hearts which are not rejected are neovascularized and begin to beat. Seventeen neonatal hearts were harvested from two litters of mice which resulted from the cross between a mouse heterozygous for the transgene and a wild type C57B1/Ka. Transplants were performed blindly into seventeen recipients. Spleen was taken from each of the neonates at the time of cardiac harvest and used for analysis of transgenic status. Of the seventeen heart harvested and transplanted, 9 were from mice expressing the transgene and 8 were from wild type littermate controls. Cardiac grafts were monitored visually every two days under 10X magnification for evidence of cardiac contractility. Mean survival time for grafts from the transgenics was 9.33 +/- 1.41 as compared to a mean survival time of 9.25 +/- 1.49 for littermate controls. This difference is not statistically significant, p = 0.9074. These data suggest that BCL-2 overexpression is not sufficient to alter allograft rejection in this model. Analysis is currently underway to assess whether allograft rejection will be affected by higher levels of BCL-2 expression or BCL-2 expression in combination with other genetic deficiencies that affect apoptotic pathways.
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