Proteome and system ontology of hemorrhagic shock: exploring early constitutive changes in postshock mesenteric lymph.
Proteome and system ontology of hemorrhagic shock: exploring early constitutive changes in postshock mesenteric lymph.
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失血性休克的蛋白质组和系统本体论：探索休克后肠系膜淋巴的早期组成变化。
DOI：
10.1016/j.surg.2009.02.022
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发表时间：
2009
期刊：
影响因子：
3.8
通讯作者：
Banerjee,Anirban
中科院分区：
文献类型：
--
作者：
Peltz,ErikD;Moore,ErnestE;Zurawel,AshleyA;Jordan,JaneenR;Damle,SagarS;Redzic,JasminaS;Masuno,Tomohiko;Eun,John;Hansen,KirkC;Banerjee,Anirban
休克后肠系膜淋巴液（PSML）是内脏缺血再灌注（IR）与远隔器官损伤之间的联系机制。我们假设，一个公正的检查PSML的蛋白质组将揭示以前未被识别的畸变系统生物学引起的血管紧张素Ⅱ诱导的肠系膜IR injury in vivo.METHODSShock在雄性SD大鼠诱导控制出血，肠系膜导管插管淋巴收集。收集休克前和休克后淋巴液进行基于差异凝胶电泳（DIGE）的蛋白质组学研究。选择相对浓度增加或减少≥1.5倍的蛋白质进行胰蛋白酶消化和质谱（MS）分析。通过PSML中细胞/组织蛋白质的增加检测组织损伤的证据。凝血成分减少，而溶血产物增加。结合珠蛋白减少，支持休克后早期溶血过程。有趣的是，几种保护性蛋白酶抑制剂在PSML中减少。意想不到的发现是α-烯醇化酶增加（一种关键的糖酵解酶和细胞表面纤溶酶原结合受体，+2.4倍变化）和主要尿蛋白增加（MUP，一种性别特异性脂质结合蛋白，+17.1倍变化）。结论PSML的蛋白质组学评价揭示了几种休克相关过程的证据：从组织损伤中释放蛋白质、凝血因子的消耗和溶血的证据、保护性蛋白酶抑制剂的消耗和脂质载体丰度的增加。这些结果表明，PSML的蛋白质组的组成性变化可能提供新的见解复杂的病理生理学休克后系统生物学。
BACKGROUNDPostshock mesenteric lymph (PSML) is the mechanistic link between splanchnic ischemia reperfusion (IR) and remote organ injury. We hypothesize that an unbiased inspection of the proteome of PSML will reveal previously unrecognized aberrations in systems biology provoked by hemorrhage-induced mesenteric IR injury in vivo.METHODSShock was induced in male Sprague-Dawley rats by controlled hemorrhage, and the mesenteric duct was cannulated for lymph collection. Preshock and postshock lymph were collected for differential in-gel electrophoresis (DIGE)-based proteomics. Proteins that increased or decreased in relative concentration ≥1.5-fold were selected for trypsin digestion and analysis by mass spectrometry (MS).RESULTSEvidence of tissue injury was detected by an increase in cell/tissue proteins in PSML. Components of coagulation were depleted, whereas products of hemolysis were increased. Haptoglobin was decreased, which supports an early postshock hemolytic process. Interestingly, several protective protease inhibitors were decreased in PSML. The unexpected findings were an increase in α-enolase (a key glycolitic enzyme and cell-surface plasminogen binding receptor, +2.4-fold change) and increased major urinary protein (MUP, a sex-specific lipid-binding protein, +17.1-fold change) in PSML.CONCLUSIONA proteomic evaluation of PSML revealed evidence of several shock-associated processes: protein release from tissue injury, depletion of coagulation factors and evidence of hemolysis, depletion of protective protease inhibitors, and an increase in abundance of lipid carriers. These results suggest that constitutive changes in the proteome of PSML may provide novel insights into the complex pathophysiology of postshock systems biology.
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DOI：
10.1097/00005373-199502000-00006
发表时间：
1995-02-01
影响因子：
--
作者：
SAUAIA, A;MOORE, FA;PONS, PT
通讯作者：
PONS, PT
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影响因子：
5.6
作者：
Martin W. Berchtold
通讯作者：
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影响因子：
4.1
作者：
A. Shiels;S. Jeffery;C. Wilson;N. Carter
通讯作者：
N. Carter
影响因子：
5.6
作者：
VANDEKERCKHOVE, J;WEBER, K
通讯作者：
WEBER, K
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影响因子：
4.8
作者：
J. Hanley;T. Haugen;E. Heath
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