Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.
Physiol Genomics. 2012 Nov 1;44(21):1027-41. doi: 10.1152/physiolgenomics.00011.2012. Epub 2012 Sep 11.
Recently we have shown that the cardioprotection afforded by cardioplegia is modulated by age and gender and is significantly decreased in the aged female. In this report we use microarray and proteomic analyses to identify transcriptomic and proteomic alterations affecting cardioprotection using cold blood cardioplegia in the mature and aged male and female heart. Mature and aged male and female New Zealand White rabbits were used for in situ blood perfused cardiopulmonary bypass. Control hearts received 30 min sham ischemia and 120 min sham reperfusion. Global ischemia (GI) hearts received 30 min of GI achieved by cross-clamping of the aorta. Cardioplegia (CP) hearts received cold blood cardioplegia prior to GI. Following 30 min of GI the hearts were reperfused for 120 min and then used for RNA and protein isolation. Microarray and proteomic analyses were performed. Functional enrichment analysis showed that mitochondrial dysfunction, oxidative phosphorylation and calcium signaling pathways were significantly enriched in all experimental groups. Glycolysis/gluconeogenesis and the pentose phosphate pathway were significantly changed in the aged male only (P < 0.05), while glyoxylate/dicarboxylate metabolism was significant in the aged female only (P < 0.05). Our data show that specific pathways associated with the mitochondrion modulate cardioprotection with CP in the aged and specifically in the aged female. The alteration of these pathways significantly contributes to decreased myocardial functional recovery and myonecrosis following ischemia and may be modulated to allow for enhanced cardioprotection in the aged and specifically in the aged female.
最近,我们已经证明,心脏停搏液提供的心脏保护作用受到年龄和性别调节,并且在老年女性中显著降低。在本报告中,我们使用微阵列和蛋白质组学分析来鉴定影响使用冷血心脏停搏液在成熟和老年雄性和雌性心脏中提供心脏保护作用的转录组和蛋白质组改变。成熟和老年雄性和雌性新西兰白兔用于原位血液灌注心肺旁路。对照心脏接受 30 分钟的假缺血和 120 分钟的假再灌注。全局缺血(GI)心脏通过夹闭主动脉接受 30 分钟的 GI。心脏停搏液(CP)心脏在 GI 前接受冷血心脏停搏液。在 30 分钟的 GI 后,心脏再灌注 120 分钟,然后用于 RNA 和蛋白质分离。进行了微阵列和蛋白质组学分析。功能富集分析表明,线粒体功能障碍、氧化磷酸化和钙信号通路在所有实验组中显著富集。仅在老年雄性中,糖酵解/糖异生和戊糖磷酸途径发生显著变化(P < 0.05),而仅在老年雌性中,乙醛酸/二羧酸代谢显著变化(P < 0.05)。我们的数据表明,与线粒体相关的特定途径调节 CP 在老年和特别是老年女性中的心脏保护作用。这些途径的改变显著导致缺血后心肌功能恢复和肌坏死减少,并且可以调节以允许在老年和特别是老年女性中增强心脏保护作用。