目的:从谷氨酸草酰乙酸转氨酶(GOT)的角度探讨急性心肌梗死(AMI)的发病机制。
方法:对20例AMI患者的血浆蛋白质组进行年龄和性别匹配,并与10例健康人进行比较。我们分析了质谱数据并比较了与其相应蛋白质相关的相应肽的信号强度。构建了样品特异性蛋白质数据库,并进行了质量控制分析,以筛选出特定实验条件下的关键调节蛋白。对37名新AMI患者和13名健康成年人的数据进行了平行反应监测(PRM),以验证发现的靶蛋白。最后,对PPI中关键基因(>1.5倍)的生存状态进行分析.
结果:对2589和2162种蛋白质进行了鉴定和定量,分别,在AMI组和对照组之间发现了143种差异表达蛋白(DEP)(≥1.5倍)。在这90和53个显著上调和下调,分别。基因本体论,KEGG浓缩,DEP的蛋白质结构域和聚类分析以及PPI网络揭示了AMI患者急性炎症反应过程的重要作用.发现一组蛋白质与半胱氨酸有关,蛋氨酸,精氨酸脯氨酸,苯丙氨酸和丙酸代谢以及cAMP信号通路。PPI网络分析显示CHI3L1、COPB2、GOT2、MB、CYCS,GOT1,CKM,SAA1和PRKCD和RPS3处于关键位置,但只有MB,CKM,GOT1PRKCD,在集群中发现CYCS和GOT2。PRM验证了MB的高水平,CKM,GOT1和GOT2在37例AMI患者中,但这些蛋白表达水平高或低的患者的生存状态没有统计学差异。
结论:我们的研究结果表明,急性炎症反应过程在AMI患者中发挥重要作用。半胱氨酸和蛋氨酸代谢也被激活,其中GOT1和GOT2是关键蛋白。这些途径可能是诊断和新疗法的潜在目标,以改善心力衰竭患者的不良预后。
OBJECTIVE: To provide a novel perspective on the pathogenesis of acute myocardial infarction (AMI) patients with respect to glutamic oxaloacetic transaminase (GOT).
METHODS: The plasma proteome of 20 patients with AMI were matched for age and sex and compared with 10 healthy individuals. We analyzed the mass spectrum data and compared the signal intensity of the corresponding peptides which related to their corresponding proteins. A sample-specific protein database was constructed and a quality control analysis was conducted to screen out the key regulatory proteins under specific experimental conditions. The data from 37 new AMI patients and 13 healthy adults were subjected to parallel reaction monitoring (PRM) to verify the target proteins found. Finally, the survival status of the key genes (> 1.5-fold) in the PPI were analyzed.
RESULTS: 2589 and 2162 proteins were identified and quantified, respectively, and 143 differentially expressed proteins (DEPs) (≥1.5-fold) were found between the AMI and control groups. Of these 90 and 53 were significantly up-regulated and down-regulated, respectively. Gene ontology, KEGG enrichment, protein domain and cluster analysis as well as PPI networks of the DEPs revealed a central role of acute inflammatory response processes in patients with AMI. A cluster of proteins were found to be related to cysteine, methionine, arginine, proline, phenylalanine and propanoate metabolism as well as the cAMP signaling pathway. PPI network analysis showed CHI3L1, COPB2, GOT2, MB, CYCS, GOT1, CKM, SAA1 and PRKCD and RPS3 were in key positions, but only MB, CKM, GOT1, PRKCD, CYCS and GOT2 were found in a cluster. PRM verified the high levels of MB, CKM, GOT1 and GOT2 in 37 AMI patients but there was no statistical difference in the survival status for patients with either high or low expression levels of these proteins.
CONCLUSIONS: Our findings showed that acute inflammatory response processes play a central role in patients with AMI. Cysteine and methionine metabolism was also activated, in which GOT1 and GOT2 were key proteins. These pathways might be potential targets for diagnosis and novel therapies to improve the poor outcomes observed in patients with heart failure.