Apolipoprotein a-I is a potential mediator of remote ischemic preconditioning.
Apolipoprotein a-I is a potential mediator of remote ischemic preconditioning.
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DOI：
10.1371/journal.pone.0077211
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Prunier F
中科院分区：
文献类型：
--
作者：
Hibert P;Prunier-Mirebeau D;Beseme O;Chwastyniak M;Tamareille S;Lamon D;Furber A;Pinet F;Prunier F
远程缺血预处理（RIPC）已成为一种有吸引力的策略在临床设置。尽管有令人信服的证据表明循环体液介质起着关键作用，但它们的实际身份仍然未知。在这项研究中，我们旨在利用蛋白质组学方法鉴定ripc诱导的体液介质。结果大鼠肢体缺血10min后再灌注5- (RIPC 5 ')或10min （RIPC 10 '）后采血。对照组只进行血液采样。采用表面增强激光解吸电离飞行时间质谱（SELDI-TOF-MS）对等离子体样品进行分析。选择了三个蛋白峰，因为它们显著增加了ripc10 '。经鉴定确认为载脂蛋白A-I （ApoA-I）。其他大鼠暴露于心肌缺血再灌注（I/R），并被分配到以下组之一：RIPC+心肌梗死（心肌I/R前20分钟开始的10分钟肢体缺血再灌注），ApoA-I+心肌梗死（心肌I/R前10分钟注射10 mg/kg ApoA-I）和心肌梗死（没有进一步干预）。与未治疗的心肌梗死大鼠相比，RIPC减少了梗死面积（RIPC+心肌梗死组为52.2±3.7%，心肌梗死组为64.9±2.6%;p<0.05）。同样，注射ApoA-I可降低梗死面积（50.9±3.8%;p<0.05）。RIPC与血浆中ApoA-I的增加有关。此外，心肌I/R前注射apoa - 1重现了RIPC对大鼠心脏的保护作用。这些数据表明apoa - 1可能是参与RIPC机制的保护性血源性因子。
Remote ischemic preconditioning (RIPC) has emerged as an attractive strategy in clinical settings. Despite convincing evidence of the critical role played by circulating humoral mediators, their actual identities remain unknown. In this study, we aimed to identify RIPC-induced humoral mediators using a proteomic approach. and Results Rats were exposed to 10-min limb ischemia followed by 5- (RIPC 5′) or 10-min (RIPC 10′) reperfusion prior to blood sampling. The control group only underwent blood sampling. Plasma samples were analyzed using surface-enhanced laser desorption and ionization - time of flight - mass spectrometry (SELDI-TOF-MS). Three protein peaks were selected for their significant increase in RIPC 10′. They were identified and confirmed as apolipoprotein A-I (ApoA-I). Additional rats were exposed to myocardial ischemia-reperfusion (I/R) and assigned to one of the following groups RIPC+myocardial infarction (MI) (10-min limb ischemia followed by 10-min reperfusion initiated 20 minutes prior to myocardial I/R), ApoA-I+MI (10 mg/kg ApoA-I injection 10 minutes before myocardial I/R), and MI (no further intervention). In comparison with untreated MI rats, RIPC reduced infarct size (52.2±3.7% in RIPC+MI vs. 64.9±2.6% in MI; p<0.05). Similarly, ApoA-I injection decreased infarct size (50.9±3.8%; p<0.05 vs. MI). RIPC was associated with a plasmatic increase in ApoA-I. Furthermore, ApoA-I injection before myocardial I/R recapitulated the cardioprotection offered by RIPC in rats. This data suggests that ApoA-I may be a protective blood-borne factor involved in the RIPC mechanism.
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作者：
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9.5
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通讯作者：
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