[1] |
Bustin M. Regulation of DNA- dependent activities by the functional motifs of the high- mobility- group chromosomal proteins[J].Mol Cell Biol,1999,19(8):5237-5246.
|
[2] |
Wang F, Lu Z, Hawkes M, et al. Fas (CD95) induces rapid,TLR4/IRAK4-dependent release of pro-inflammatory HMGB1 from macrophages[J].Inflamm(Lond),2010,17(7):30.
|
[3] |
Thomas JO, Travesr AA. HMG1 and 2, and related'architectural' DNA-binding proteins[J]. Trends Biochem Sci,2001,26(3):167-174.
|
[4] |
Gong W,Zheng Y,Chao F,et al.The anti-inflammatory activity of HMGB1 A box is enhanced when fused with C-terminal acidic tail[J].J Biomed Biotechnol,2010,2010:915234.
|
[5] |
Yang H, Antoine DJ, Andersson U, et al. The many faces of HMGB1: molecular structure- functional activity in inflammation, apoptosis, and chemotaxis[J]. J Leukoc Biol,2013,93(6):865-873.
|
[6] |
Wang JG, Bondy SC, Zhou L, et al. Protective effect of Tanshinone IIA against infarct size and increased HMGB1,NFκB, GFAP and apoptosis consequent to transient middle cerebral artery occlusion[J]. Neurochem Res, 2014, 39(2):295-304.
|
[7] |
Nakahara T, Tsuruta R, Kaneko T, et al. High-mobility group box 1 protein in CSF of patients with subarachnoid hemorrhage[J].Neurocrit Care,2009,11(3):362-368.
|
[8] |
Li M, Sun L, Luo Y, et al. High-mobility group box 1 released from astrocytes promotes the proliferation of cultured neural stem/progenitor cells[J].Int J Mol Med,2014,34(3):705-714.
|
[9] |
Wang H, Bloom O, Zhang M, et al. HMG-1 as a late mediator of endotoxin lethality in mice[J]. Science, 1999, 285(5425):248-251.
|
[10] |
Gardella S, Andrei C, Ferrera D, et al. The nuclear protein HMB1 is secreted by monocytes via a non- classical,vesicle- mediated secretory pathway[J]. EMBO Rep, 2002,3(10):995-1001.
|
[11] |
Lamkanfi M, Sarkar A, Vande WL et al, Inflammasome dependent release of the alarmin HMGB1 in endotoxemia[J]. J Immunol,2010,185(7):4385-4392.
|
[12] |
Yang S, Xu L, Yang T, Wang F. et al. High-mobility group box-1 and its role in angiogenesis[J]. J Leukoc Biol, 2014, 95(4):563-574.
|
[13] |
Scaffidi P,Misteli T,Bianchi ME.Release of chromatin protein HMGB1 by necrotic cells triggers inflammation[J]. Nature,2002,418(6894):191-195.
|
[14] |
Andersson U, Tracey KJ. HMGB1 is a therapeutic target for sterile inflammation and infection[J]. Annu Rev Immunol,2011,29:139-162.
|
[15] |
Pisetsky D.Cell death in the pathogenesis of immune-mediated diseases: the role of HMGB1 and DAMP-PAMP complexes[J].Swiss Med Wkly,2011,141:w13256.
|
[16] |
Harris HE, Andersson U, Pisetsky DS. HMGB1: a multifunctional alarmin driving autoimmune and inflammatory disease[J].Nat Rev Rheumatol,2012,8(4):195-202.
|
[17] |
Keyel PA.How is inflammation initiated?Individual influences of IL-1,IL-18 and HMGB1[J].Cytokine,2014,69(1):136-145.
|
[18] |
Fucikova J, Kralikova P, FiaIova A, et al. Human tumor cells killed by anthracyclines induce a tumor- specific immune response[J].Cancer Res,2011,71(14):4821-4833.
|
[19] |
RauvalaH,RouhiainenA.Physiologicaland pathophysiological outcomes of the interactions of HMGB1 with cell surface receptors[J]. Biochim Biophys Acta, 2010,1799(1-2):164-170.
|
[20] |
Urbonaviciute V, Fumrohr BG, Meister S, et al. Induction of inflammatory and immune responses by HMGBl-nucleosome complexes: implications for the pathogenesis of SLE[J]. Exp Med,2008,205(13):3007-3018.
|
[21] |
Nortje J, Menon DK. Traumatic brain injury: physiology,mechanisms, and outcome[J]. Curr Opin Neurol, 2004, 17(6):711-718.
|
[22] |
Maas AI, Marmarou A, Murray GD, et al. Prognosis and clinical trial design in traumatic brain injury:the IMPACT study[J].J Neurotrauma,2007,24(2):232-238..
|
[23] |
Wang YC, Lin S, Yang QW. Toll-like receptors in cerebral ischemic inflammatory injury[J]. J Neuroinflammation, 2011,8:134.
|
[24] |
Vogelgesang A, May VE, Grunwald U, et al. Functional status of peripheral blood T-cells in ischemic stroke patients[J]. PLoS One,2010,5(1):e8718.
|
[25] |
Okuma Y, Liu K, Wake H, et al. Anti-high mobility group box- 1 antibody therapy for traumatic brain injury[J]. Ann Neurol,2012,72(3):373-384.
|
[26] |
Laird MD, Shields JS, Sukumari- Ramesh S, et al. High mobility group box protein-1 promotes cerebral edema after traumatic brain injury via activation of toll-like receptor 4[J].Glia,2014,62(1):26-38.
|
[27] |
Feigin VL, Lawes CM, Bennett DA, et al. Stroke epidemiology: a review of population- based studies of incidence, prevalence, and case-fatality in the late 20th century[J].Lancet Neurol,2(1):43-53.
|
[28] |
Yang QW, Lu FL, Zhou Y, et al. HMBG1 mediates ischemia reperfusion injury by TRIF- adaptor independent Toll- like receptor 4 signaling[J]. J Cereb Blood Flow Metab, 2011, 31(2):593-605.
|
[29] |
Xiong XX, Gu LJ, Shen J, et al. Probenecid protects against transient focal cerebral ischemic injury by inhibiting HMGB1 release and attenuating AQP4 expression in mice[J].Neurochem Res,2014,39(1):216-224.
|
[30] |
Kim SW, Lim CM, Kim JB, et al. Extracellular HMGB1 Released by NMDA Treatment Confers Neuronal Apoptosis via RAGE-p38 MAPK/ERK Signaling Pathway[J]. Neurotox Res,2011,20(2):159-169.
|
[31] |
Lee JC, Cho GS, Choi BO, et al. Intracerebral hemorrhage induced brain injury is aggravated in senescence-accelerated prone mice[J].Stroke,2006,37(1):216-222.董钊,石铸,王璐,等.高血压脑出血患者急性期血肿周围组织的炎症反应特征[J]. 临床神经病学杂志, 2007, 20(4):249-251.
|
[33] |
Lei C, Lin S, Zhang C et al. High-mobility group box1 protein promotes neuroinflammation after intracerebral hemorrhage in rats[J].Neuroscience,2013,228:190-199.
|
[34] |
Sun Q, Wu W, Hu YC, et al. Early release of high-mobility group box 1(HMGB1) from neurons in experimental subarachnoid hemorrhage in vivo and in vitro[J].Neuroinflammation,2014,11:106.
|