[1] 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.
[2] Lamkanfi M, Sarkar A, Vande Walle L, et al. Inflammasome-dependent release of the alarmin HMGB1 in endotoxemia [J]. J Immunol, 2010, 185(7):4385-4392.
[3] Buhimschi CS, Baumbusch MA, Dulay AT, et al. Characterization of RAGE, HMGB1, and S100beta in inflammation-induced Preterm birth and fetal tissue injury[J]. Am J Pathol, 2009,175(3):958-975.
[4] Sundberg E, Fasth AE, Palmblad K, et al. High mobility group box chromosomal protein 1 acts as a proliferation signal for activated T lymphocytes [J]. Immunobiology, 2009, 214(4):303-309.
[5] Munoz-Planillo R, Franchi L, Miller LS, et al. A critical role for hemolysins and bacterial lipoproteins in Staphylococcus aureus-induced activation of the Nlrp3 inflammasome [J]. J Immunol, 2009, 183(6):3942-3948.
[6] Willingham SB, Allen IC, Bergstralh DT, et al. NLRP3 (NALP3, Cryopyrin) facilitates in vivo caspase-1 activation, necrosis, and HMGB1 release via inflammasome-dependent and -independent pathways[J]. J Immunol, 2009, 183(3):2008-2015.
[7] Lamkanfi M, Dixit VM. Manipulation of host cell death pathways during microbial infections[J]. Cell Host Microbe, 2010, 8(1):44-54.
[8] Evasic R, Block C. Fixture modification and osseous regeneration of the "ailing/failing" implant [J]. J Oral Impant, 1999, 25(2):135-137.
[9] Andersson U, Wang H, Palmblad K, et a1. High mobility group1 protein (HMG-1) stimulates proinflammatory cytokine synthesis in human monocytes[J]. J Exp Med, 2000, 192(4):565-570.
[10] Lutterloh EC, Opal SM, Pittman DD, et al. Inhibition of the RAGE products increases survival in experimental models of severe sepsis and systemic infection[J]. Crit Care, 2007, 11(2):R122.
[11] Park JS, Svetkauskaite D, He Q, et al. Involvement of toll-like receptors 2 and 4 in cellular activation by high mobility group box l protein[J]. J Biol Chem, 2004, 279(9):7370-7377.
[12] DeMarco RA, Fink MP, Lotze MT. Monocytes promote natural killer cell interferon gamma production in response to the endogenous danger signal HMGB1[J]. Mol Immunol,2005,42(4):433-444.
[13] Palumbo R, Sampaolesi M, De Marchis F, et al. Extracellular HMGB 1, a signal of tissue damage, induces mesoangioblast migration and proliferation[J]. J Cell Biol, 2004, 164(3):441-449.
[14] Morimoto Y, Kawahara KI, Tancharoen S, et al. Tumor necrosis factor-alpha stimulates gingival epithelial cells to release high mobility-group box 1[J]. J Periodontal Res, 2008, 43(1):76-83.
[15] Luo L, Xie P, Gong P, et al. Expression of HMGB1 and HMGN2 in gingival tissues, GCF and PICF of periodontitis patients and peri-implantitis[J]. Arch Oral Biol, 2011,56(10):1106-1111.
[16] Petkovic AB, Matic SM, Stamatovic NV, et al. Proinflammatory cytokines (IL-1beta and TNF-alpha) and chemokines (IL-8 and MIP-1alpha) as markers of peri-implant tissue condition[J]. Int J Oral Maxillofac Surg, 2010,39(5):478-485.
[17] Ito Y, Bhawal UK, Sasahira T, et al. Involvement of HMGB1 and RAGE in IL-1β-induced gingival inflammation[J]. Arch Oral Biol, 2012,57(1):73-80. |