Remote ischemic preconditioning (RIPC) modifies the plasma proteome in children undergoing repair of tetralogy of fallot: a randomized controlled trial.
Remote ischemic preconditioning (RIPC) modifies the plasma proteome in children undergoing repair of tetralogy of fallot: a randomized controlled trial.
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DOI：
10.1371/journal.pone.0122778
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Konstantinov IE
中科院分区：
文献类型：
--
作者：
Hepponstall M;Ignjatovic V;Binos S;Attard C;Karlaftis V;d'Udekem Y;Monagle P;Konstantinov IE
远程缺血预处理（RIPC）已应用于小儿心脏手术。我们已经证明，RIPC诱导健康志愿者血浆中的蛋白质组学反应。我们测试了RIPC改变接受法洛四联症（TOF）修复的儿童蛋白质组反应的假设。将40名儿童随机分为RIPC组和对照组。在基线、体外循环（CPB）后和CPB后6、12和24 h采集血液。通过液相色谱质谱法（LC-MS）以非靶向方法分析血浆。对显示差异表达（p<0.01）的肽进行串联LC-MS/MS和蛋白质鉴定。使用NCBI蛋白质数据库鉴定相应的蛋白质。年龄（7.3± 3.5 vs 6.8 ±3.6个月）（p=0.89）、体重（7.7± 1.8 vs 7.5 ±1.9 kg）（p=0.71）、CPB时间（104± 7 vs 94 ±7 min）（p=0.98）或主动脉阻断时间（83± 22 vs 75 ±20 min）（p=0.36）无差异。在基线或CPB后立即没有肽差异表达。体外循环后6 h，RIPC组有48种肽表达较高。这在12或24小时时不再明显，其中一种肽在RIPC组中下调。鉴定的蛋白质为：间α球蛋白抑制剂（42.0±11.8 vs 820.8±181.1，p=0.006），纤维蛋白原前蛋白原（59.3±11.2 vs 1192.6±278.3，p=0.007），补体C3前体（391.2±160.9 vs 5385.1±689.4，p=0.0005），补体C4 B（151.5±17.8 vs 4587.8±799.2，p=0.003），载脂蛋白B100（53.4±8.3 vs 1364.5±278.2，p=0.005）和尿蛋白酶抑制剂（358.6±74.9 vs 5758.1±1343.1，p=0.009）。这些蛋白质参与代谢、止血、免疫和炎症。我们提供了第一个全面分析RIPC诱导的蛋白质组学变化的儿童接受手术。蛋白质组学变化在CPB后6小时达到峰值，并在手术后24小时内恢复至基线。ACTR.org.au ACTRN12610000496011
Remote ischemic preconditioning (RIPC) has been applied in paediatric cardiac surgery. We have demonstrated that RIPC induces a proteomic response in plasma of healthy volunteers. We tested the hypothesis that RIPC modifies the proteomic response in children undergoing Tetralogy of Fallot (TOF) repair. Children (n=40) were randomized to RIPC and control groups. Blood was sampled at baseline, after cardiopulmonary bypass (CPB) and 6, 12 and 24h post-CPB. Plasma was analysed by liquid chromatography mass spectrometry (LC-MS) in an untargeted approach. Peptides demonstrating differential expression (p<0.01) were subjected to tandem LC-MS/MS and protein identification. Corresponding proteins were identified using the NCBI protein database. There was no difference in age (7.3±3.5vs6.8±3.6 months)(p=0.89), weight (7.7±1.8vs7.5±1.9 kg)(p=0.71), CPB time (104±7vs94±7 min)(p=0.98) or aortic cross-clamp time (83±22vs75±20 min)(p=0.36). No peptides were differentially expressed at baseline or immediately after CPB. There were 48 peptides with higher expression in the RIPC group 6h post-CPB. This was no longer evident at 12 or 24h, with one peptide down-regulated in the RIPC group. The proteins identified were: inter-alpha globulin inhibitor (42.0±11.8 vs 820.8±181.1, p=0.006), fibrinogen preproprotein (59.3±11.2 vs 1192.6±278.3, p=0.007), complement-C3 precursor (391.2±160.9 vs 5385.1±689.4, p=0.0005), complement C4B (151.5±17.8 vs 4587.8±799.2, p=0.003), apolipoprotein B100 (53.4±8.3 vs 1364.5±278.2, p=0.005) and urinary proteinase inhibitor (358.6±74.9 vs 5758.1±1343.1, p=0.009). These proteins are involved in metabolism, haemostasis, immunity and inflammation. We provided the first comprehensive analysis of RIPC-induced proteomic changes in children undergoing surgery. The proteomic changes peak 6h post-CPB and return to baseline within 24h of surgery. ACTR.org.au ACTRN12610000496011
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