期刊论文详细信息
Journal of Neuroinflammation
Relationship between plasma high mobility group box-1 protein levels and clinical outcomes of aneurysmal subarachnoid hemorrhage
Jian-Min Zhang1  Gao Chen1  Qi-Chang Liu1  Feng Zhou1  Jing-Sen Chen1  Xiang-Dong Zhu1 
[1] Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, 88 Jiefang Road, Hangzhou, 310000, PR China
关键词: Mortality;    High-mobility group box 1;    Functional outcome;    Cerebrovasospasm;    Aneurysmal subarachnoid hemorrhage;   
Others  :  1160313
DOI  :  10.1186/1742-2094-9-194
 received in 2012-04-06, accepted in 2012-07-24,  发布年份 2012
PDF
【 摘 要 】

Background

High-mobility group box 1 (HMGB1), originally described as a nuclear protein that binds to and modifies DNA, is now regarded as a central mediator of inflammation by acting as a cytokine. However, the association of HMGB1 in the peripheral blood with disease outcome and cerebrovasospasm has not been examined in patients with aneurysmal subarachnoid hemorrhage.

Methods

In this study, 303 consecutive patients were included. Upon admission, plasma HMGB1 levels were measured by ELISA. The end points were mortality after 1 year, in-hospital mortality, cerebrovasospasm and poor functional outcome (Glasgow Outcome Scale score of 1 to 3) after 1 year.

Results

Upon admission, the plasma HMGB1 level in patients was statistically significantly higher than that in healthy controls. A multivariate analysis showed that the plasma HMGB1 level was an independent predictor of poor functional outcome and mortality after 1 year, in-hospital mortality and cerebrovasospasm. A receiver operating characteristic curve showed that plasma HMGB1 level on admission statistically significantly predicted poor functional outcome and mortality after 1 year, in-hospital mortality and cerebrovasospasm of patients. The area under the curve of the HMGB1 concentration was similar to those of World Federation of Neurological Surgeons (WFNS) score and modified Fisher score for the prediction of poor functional outcome and mortality after 1 year, and in-hospital mortality, but not for the prediction of cerebrovasospasm. In a combined logistic-regression model, HMGB1 improved the area under the curve of WFNS score and modified Fisher score for the prediction of poor functional outcome after 1 year, but not for the prediction of mortality after 1 year, in-hospital mortality, or cerebrovasospasm.

Conclusions

HMGB1 level is a useful, complementary tool to predict functional outcome and mortality after aneurysmal subarachnoid hemorrhage. However, HMGB1 determination does not add to the accuracy of prediction of the clinical outcomes.

【 授权许可】

   
2012 Zhu et al.; licensee BioMed Central Ltd.

【 预 览 】
附件列表
Files Size Format View
20150410101746437.pdf 575KB PDF download
Figure 2. 98KB Image download
Figure 1. 57KB Image download
【 图 表 】

Figure 1.

Figure 2.

【 参考文献 】
  • [1]Liebenberg WA, Worth R, Firth GB, Olney J, Norris JS: Aneurysmal subarachnoid haemorrhage: guidance in making the correct diagnosis. Postgrad Med J 2005, 81:470-473.
  • [2]Drake C: Report of world federation of neurological surgeons committee on a universal subarachnoid hemorrhage grading scale. J Neurosurg 1988, 68:985-986.
  • [3]Fisher CM, Kistler JP, Davis JM: Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery 1980, 6:1-9.
  • [4]Turck N, Vutskits L, Sanchez-Pena P, Robin X, Hainard A, Gex-Fabry M, Fouda C, Bassem H, Mueller M, Lisacek F, Puybasset L, Sanchez JC: A multiparameter panel method for outcome prediction following aneurysmal subarachnoid hemorrhage. Intensive Care Med 2010, 36:107-115.
  • [5]Goodwin GH, Sanders C, Johns EW: A new group of chromatin-associated proteins with a high content of acidic and basic amino acids. Eur J Biochem 1973, 38:14-19.
  • [6]Javaherian K, Liu JF, Wang JC: Nonhistone proteins HMG1 and HMG2 change the DNA helical structure. Science 1978, 199:1345-1346.
  • [7]Wang H, Bloom O, Zhang M, Vishnubhakat JM, Ombrellino M, Che J, Frazier A, Yang H, Ivanova S, Borovikova L, Manogue KR, Faist E, Abraham E, Andersson J, Andersson U, Molina PE, Abumrad NN, Sama A, Tracey KJ: HMG-1 as a late mediator of endotoxin lethality in mice. Science 1999, 285:248-251.
  • [8]Scaffidi P, Misteli T, Bianchi ME: Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature 2002, 418:191-195.
  • [9]Lotze MT, Tracey KJ: High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal. Nat Rev Immunol 2005, 5:331-342.
  • [10]Dumitriu IE, Baruah P, Manfredi AA, Bianchi ME, Rovere-Querini P: HMGB1: guiding immunity from within. Trends Immunol 2005, 26:381-387.
  • [11]Bianchi ME, Manfredi AA: High-mobility group box 1 (HMGB1) protein at the crossroads between innate and adaptive immunity. Immunol Rev 2007, 220:35-46.
  • [12]Klune JR, Dhupar R, Cardinal J, Billiar TR, Tsung A: HMGB1: endogenous danger signaling. Mol Med 2008, 14:476-484.
  • [13]Guazzi S, Strangio A, Franzi AT, Bianchi ME: HMGB1, an architectural chromatin protein and an extracellular signaling factor, has a spatially and temporally restricted expression pattern in mouse brain. Gene Expr Patterns 2003, 3:29-33.
  • [14]Watanabe M, Miyajima M, Nakajima M, Arai H, Ogino I, Nakamura S, Kunichika M: Expression analysis of high mobility group box-1 protein (HMGB-1) in the cerebral cortex, hippocampus, and cerebellum of the congenital hydrocephalus (H-Tx) rat. Acta Neurochir Suppl 2012, 113:91-96.
  • [15]Murakami K, Koide M, Dumont TM, Russell SR, Tranmer BI, Wellman GC: Subarachnoid hemorrhage induces gliosis and increased expression of the pro-inflammatory cytokine high mobility group box 1 protein. Transl Stroke Res 2011, 2:72-79.
  • [16]Agnello D, Wang H, Yang H, Tracey KJ, Ghezzi P: HMGB-1, a DNA-binding protein with cytokine activity, induces brain TNF and IL-6 production, and mediates anorexia and taste aversion. Cytokine 2002, 18:231-236.
  • [17]Kim JB, Sig Choi J, Yu YM, Nam K, Piao CS, Kim SW, Lee MH, Han PL, Park JS, Lee JK: HMGB1, a novel cytokine-like mediator linking acute neuronal death and delayed neuroinflammation in the postischemic brain. J Neurosci 2006, 26:6413-6421.
  • [18]O'Connor KA, Hansen MK, Rachal Pugh C, Deak MM, Biedenkapp JC, Milligan ED, Johnson JD, Wang H, Maier SF, Tracey KJ, Watkins LR: Further characterization of high mobility group box 1 (HMGB1) as a proinflammatory cytokine: central nervous system effects. Cytokine 2003, 24:254-265.
  • [19]Takata K, Kitamura Y, Kakimura J, Shibagaki K, Tsuchiya D, Taniguchi T, Smith MA, Perry G, Shimohama S: Role of high mobility group protein-1 (HMG1) in amyloid-beta homeostasis. Biochem Biophys Res Commun 2003, 301:699-703.
  • [20]Takata K, Kitamura Y, Tsuchiya D, Kawasaki T, Taniguchi T, Shimohama S: High mobility group box protein-1 inhibits microglial Abeta clearance and enhances Abeta neurotoxicity. J Neurosci Res 2004, 78:880-891.
  • [21]Pedrazzi M, Patrone M, Passalacqua M, Ranzato E, Colamassaro D, Sparatore B, Pontremoli S, Melloni E: Selective proinflammatory activation of astrocytes by high-mobility group box 1 protein signaling. J Immunol 2007, 179:8525-8532.
  • [22]Tang D, Kang R, Cao L, Zhang G, Yu Y, Xiao W, Wang H, Xiao X: A pilot study to detect high mobility group box 1 and heat shock protein 72 in cerebrospinal fluid of pediatric patients with meningitis. Crit Care Med 2008, 36:291-295.
  • [23]Goldstein RS, Gallowitsch-Puerta M, Yang L, Rosas-Ballina M, Huston JM, Czura CJ, Lee DC, Ward MF, Bruchfeld AN, Wang H, Lesser ML, Church AL, Litroff AH, Sama AE, Tracey KJ: Elevated high-mobility group box 1 levels in patients with cerebral and myocardial ischemia. Shock 2006, 25:571-574.
  • [24]Nakahara T, Tsuruta R, Kaneko T, Yamashita S, Fujita M, Kasaoka S, Hashiguchi T, Suzuki M, Maruyama I, Maekawa T: High-mobility group box 1 protein in CSF of patients with subarachnoid hemorrhage. Neurocrit Care 2009, 11:362-368.
  • [25]King MD, Laird MD, Ramesh SS, Youssef P, Shakir B, Vender JR, Alleyne CH, Dhandapani KM: Elucidating novel mechanisms of brain injury following subarachnoid hemorrhage: an emerging role for neuroproteomics. Neurosurg Focus 2010, 28:E10.
  • [26]Jennett B, Bond M: Assessment of outcome after severe brain damage. Lancet 1975, 1:480-484.
  • [27]Landsman D, Bustin MA: Signature for the HMG-1 box DNA-binding proteins. Bioessays 1993, 15:539-546.
  • [28]Bustin M: Regulation of DNA-dependent activities by the functional motifs of the high-mobility-group chromosomal proteins. Mol Cell Biol 1999, 19:5237-5246.
  • [29]Abraham E, Arcaroli J, Carmody A, Wang H, Tracey KJ: HMG-1 as a mediator of acute lung inflammation. J Immunol 2000, 165:2950-2954.
  • [30]Bonaldi T, Talamo F, Scaffidi P, Ferrera D, Porto A, Bachi A, Rubartelli A, Agresti A, Bianchi ME: Monocytic cells hyperacetylate chromatin protein HMGB1 to redirect it towards secretion. EMBO J 2003, 22:5551-5560.
  • [31]Yang H, Ochani M, Li J, Qiang X, Tanovic M, Harris HE, Susarla SM, Ulloa L, Wang H, DiRaimo R, Czura CJ, Wang H, Roth J, Warren HS, Fink MP, Fenton MJ, Andersson U, Tracey KJ: Reversing established sepsis with antagonists of endogenous high-mobility group box 1. Proc Natl Acad Sci USA 2004, 101:296-301.
  • [32]Ombrellino M, Wang H, Ajemian MS, Talhouk A, Scher LA, Friedman SG, Tracey KJ: Increased serum concentrations of high-mobility group protein 1 in haemorrhagic shock. Lancet 1999, 354:1446-1447.
  • [33]Wang H, Vishnubhakat JM, Bloom O, Zhang M, Ombrellino M, Sama A, Tracey KJ: Proinflammatory cytokines (tumor necrosis factor and interleukin 1) stimulate release of high mobility group protein-1 by pituicytes. Surgery 1999, 126:389-392.
  • [34]Huttunen HJ, Fages C, Rauvala H: Receptor for advanced glycation end products (RAGE)-mediated neurite outgrowth and activation of NF-kB require the cytoplasmic domain of the receptor but different downstream signaling pathways. J Biol Chem 1999, 274:19919-19924.
  • [35]Taguchi A, Blood DC, del Toro G, Canet A, Lee DC, Qu W, Tanji N, Lu Y, Lalla E, Fu C, Hofmann MA, Kislinger T, Ingram M, Lu A, Tanaka H, Hori O, Ogawa S, Stern DM, Schmidt AM: Blockade of RAGE amphoterin signalling suppresses tumour growth and metastases. Nature 2000, 405:354-360.
  • [36]Park JS, Arcaroli J, Yum HK, Yang H, Wang H, Yang KY, Choe KH, Strassheim D, Pitts TM, Tracey KJ, Abraham E: Activation of gene expression in human neutrophils by high mobility group box 1 protein. Am J Physiol Cell Physiol 2003, 284:C870-C879.
  • [37]Schmidt AM, Yan SD, Yan SF, Stern DM: The biology of the receptor for advanced glycation end products and its ligands. Biochim Biophys Acta 2000, 1498:99-111.
  • [38]Huttunen HJ, Rauvala H: Amphoterin as an extracellular regulator of cell motility: from discovery to disease. J Int Med 2004, 255:351-366.
  • [39]Park JS, Svetkauskaite D, He Q, Kim JY, Strassheim D, Ishizaka A, Abraham E: Involvement of Toll-like receptors 2 and 4 in cellular activation by high mobility group box 1 protein. J Biol Chem 2004, 279:7370-7377.
  • [40]Tsung A, Sahai R, Tanaka H, Nakao A, Fink MP, Lotze MT, Yang H, Li J, Tracey KJ, Geller DA, Billiar TR: The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion. J Exp Med 2005, 201:1135-1143.
  • [41]Muhammad S, Barakat W, Stoyanov S, Murikinati S, Yang H, Tracey KJ, Bendszus M, Rossetti G, Nawroth PP, Bierhaus A, Schwaninger M: The HMGB1 receptor RAGE mediates ischemic brain damage. J Neurosci 2008, 28:12023-12031.
  • [42]Sobey CG, Faraci FM: Subarachnoid haemorrhage: what happens to the cerebral arteries? Clin Exp Pharmacol Physiol 1998, 25:867-876.
  • [43]Cook DA: Mechanisms of cerebral vasospasm in subarachnoid haemorrhage. Pharmacol Ther 1995, 66:259-284.
  • [44]Hansen-Schwartz J, Vajkoczy P, Macdonald RL, Pluta RM, Zhang JH: Cerebral vasospasm: looking beyond vasoconstriction. Trends Pharmacol Sci 2007, 28:252-256.
  • [45]Pluta RM, Hansen-Schwartz J, Dreier J, Vajkoczy P, Macdonald RL, Nishizawa S, Kasuya H, Wellman G, Keller E, Zauner A, Dorsch N, Clark J, Ono S, Kiris T, Leroux P, Zhang JH: Cerebral vasospasm following subarachnoid hemorrhage: time for a new world of thought. Neurol Res 2009, 31:151-158.
  • [46]Sabri M, Kawashima A, Ai J, Macdonald RL: Neuronal and astrocytic apoptosis after subarachnoid hemorrhage: a possible cause for poor prognosis. Brain Res 2008, 1238:163-171.
  • [47]Vergouwen MD, Vermeulen M, Coert BA, Stroes ES, Roos YB: Microthrombosis after aneurysmal subarachnoid hemorrhage: an additional explanation for delayed cerebral ischemia. J Cereb Blood Flow Metab 2008, 28:1761-1770.
  • [48]Wellman GC: Ion channels and calcium signaling in cerebral arteries following subarachnoid hemorrhage. Neurol Res 2006, 28:690-702.
  • [49]Skrha J, Kalousová M, Svarcová J, Muravská A, Kvasnička J, Landová L, Zima T, Skrha J: Relationship of soluble RAGE and RAGE ligands HMGB1 and EN-RAGE to endothelial dysfunction in Type 1 and Type 2 diabetes mellitus. Exp Clin Endocrinol Diabetes 2012, 120:277-281.
  • [50]Haraba R, Uyy E, Suica VI, Ivan L, Antohe F: Fluvastatin reduces the high mobility group box 1 protein expression in hyperlipidemia. Int J Cardiol 2011, 150:105-107.
  • [51]Tang D, Kang R, Zeh HJ, Lotze MT: High-mobility group box 1, oxidative stress, and disease. Antioxid Redox Signal 2011, 14:1315-1335.
  • [52]Ding HS, Yang J: High mobility group box-1 and cardiovascular diseases. Saudi Med J 2010, 31:486-489.
  文献评价指标  
  下载次数:0次 浏览次数:3次