AI Chat Paper
Note: Please note that the following content is generated by AMiner AI. SciOpen does not take any responsibility related to this content.
{{lang === 'zh_CN' ? '文章概述' : 'Summary'}}
{{lang === 'en_US' ? '中' : 'Eng'}}
Chat more with AI
PDF (937 KB)
Collect
Submit Manuscript AI Chat Paper
Show Outline
Outline
Show full outline
Hide outline
Outline
Show full outline
Hide outline
Review Article | Open Access

Inflammatory signaling of HMGB1 in depressive disorder

Qian JiangChaoran LiHuijing XuTaosheng LiuYunxia Wang( )
Faculty of Psychology, Naval Medical University, Shanghai 200433, China
Show Author Information

Abstract

Background:

Depressive disorder is a common disease characterized by depressed mood and loss of pleasure, which often brings a great grief to patients and a huge burden to the society. Currently, the therapeutic strategy has made a rapid progress, but even the most well-studied and commonly used antidepressants will take weeks to produce a desired effect and have some side-effects. Besides, the objective and specific diagnostic indexes are still absent. Many important hypotheses have been proposed and inflammation is one of them. Among the inflammatory cytokines that might be closely related to depression, HMGB1 is a novel and vital one.

Methods:

We reviewed and analyzed literature on PubMed and web of science using the relevant key words ( "depression/MDD" in conjunction with "HMGB1/high mobility group box 1).

Results:

We found that both clinical and laboratory studies demonstrated pro-inflammatory role of HMGB1 in depressive disorder, while conditional knockout or inhibition of HMGB1 could alleviate inflammation and depression.

Conclusion:

Therefore, in this review we will talk about the possible role of HMGB1 in the development of depressive disorder and the underlying mechanisms with the hope of providing evidence for a novel and effective therapy for depressive disorder.

References

[1]
Reed, G. M., First, M. B., Kogan, C. S., Hyman, S. E., Gureje, O., Gaebel, W., Maj, M., Stein, D. J., Maercker, A., Tyrer, P. et al. Innovations and changes in the ICD-11 classification of mental, behavioural and neurodevelopmental disorders. Asian Journal of Andrology, 2019, 18(1): 3–19.
[2]
Huang, Y., Wang, Y., Wang, H., Liu, Z., Yu, X., Yan, J., Yu, Y., Kou, C., et al. Prevalence of mental disorders in China: A cross-sectional epidemiological study. The Lancet Psychiatry, 2019, 6(3): 211–224.
[3]
GBD 2017 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990-2017: A systematic analysis for the Global Burden of Disease Study 2017. The Lancet, 2018, 392(10159): 1789–1858.
[4]
Boschloo, L., Schoevers, R. A., Beekman, A. T. F., Smit, J. H., van Hemert, A. M., Penninx, B. W. J. H. The four-year course of major depressive disorder: The role of staging and risk factor determination. Psychotherapy and Psychosomatics, 2014, 83(5): 279–288.
[5]
Spijker, J., de Graaf, R., Bijl, R. V., Beekman, A. T. F., Ormel, J., Nolen, W. A. Determinants of persistence of major depressive episodes in the general population. Results from the Netherlands Mental Health Survey and Incidence Study (NEMESIS). Journal of Affective Disorders, 2004, 81(3): 231–240.
[6]
Undurraga, J., Baldessarini, R. J. Direct comparison of tricyclic and serotonin-reuptake inhibitor antidepressants in randomized head-to-head trials in acute major depression: Systematic review and meta-analysis. Journal of Psychopharmacology (Oxford, England), 2017, 31(9): 1184–1189.
[7]
Moret, C., Isaac, M., Briley, M. Review: Problems associated with long-term treatment with selective serotonin reuptake inhibitors. Journal of Psychopharmacology, 2009, 23(8): 967–974.
[8]
Malhi, G. S., Mann, J. J. Depression. The Lancet, 2018, 392(10161): 2299–2312.
[9]
Choi, K., Chun, J., Han, K., Park, S., Soh, H., Kim, J., Lee, J., Lee, H. J., Im, J. P., Kim, J. S. Risk of anxiety and depression in patients with inflammatory bowel disease: A nationwide, population-based study. Journal of Clinical Medicine, 2019, 8(5): 654.
[10]
Semenkovich, K., Brown, M. E., Svrakic, D. M., Lustman, P. J. Depression in type 2 diabetes mellitus: Prevalence, impact, and treatment. Drugs, 2015, 75(6): 577–587.
[11]
Nerurkar, L., Siebert, S., McInnes, I. B., Cavanagh, J. Rheumatoid arthritis and depression: An inflammatory perspective. The Lancet Psychiatry, 2019, 6(2): 164–173.
[12]
Paudel, Y. N., Angelopoulou, E., Piperi, C., Othman, I., Aamir, K., Shaikh, M. F. Impact of HMGB1, RAGE, and TLR4 in alzheimer’s disease (AD): From risk factors to therapeutic targeting. Cells, 2020, 9(2): 383.
[13]
Leighton, S. P., Nerurkar, L., Krishnadas, R., Johnman, C., Graham, G. J., Cavanagh, J. Chemokines in depression in health and in inflammatory illness: A systematic review and meta-analysis. Molecular Psychiatry, 2018, 23(1): 48–58.
[14]
Pape, K., Tamouza, R., Leboyer, M., Zipp, F. Immunoneuropsychiatry—novel perspectives on brain disorders. Nature Reviews Neurology, 2019, 15(6): 317–328.
[15]
Chamberlain Samuel, R., Jonathan, C., Peter, D. B., Valeria, M., Jones Declan, N. C., Drevets Wayne, C., Cowen Philip, J., Harrison Neil, A., Linda, P., Pariante Carmine, M. et al. Treatment-resistant depression and peripheral C-reactive protein. The British Journal of Psychiatry: the Journal of Mental Science, 2019, 214(1): 11–19.
[16]
Friebe, A., Horn, M., Schmidt, F., Janssen, G., Schmid-Wendtner, M. H., Volkenandt, M., Hauschild, A., Goldsmith, C. H., Schaefer, M. Dose-dependent development of depressive symptoms during adjuvant interferon-treatment of patients with malignant melanoma. Psychosomatics, 2010, 51(6): 466–473.
[17]
Fourrier, C., Sampson, E., Mills, N. T., Baune, B. T. Anti-inflammatory treatment of depression: Study protocol for a randomised controlled trial of vortioxetine augmented with celecoxib or placebo. Trials, 2018, 19(1): 447.
[18]
Rosenblat, J. D., Kakar, R., Berk, M., Kessing, L. V., Vinberg, M., Baune, B. T., Mansur, R. B., Brietzke, E., Goldstein, B. I., McIntyre, R. S. Anti-inflammatory agents in the treatment of bipolar depression: A systematic review and meta-analysis. Bipolar Disorders, 2016, 18(2): 89–101.
[19]
Köhler, O., Benros, M. E., Nordentoft, M., Farkouh, M. E., Iyengar, R. L., Mors, O., Krogh, J. Effect of anti-inflammatory treatment on depression, depressive symptoms, and adverse effects. JAMA Psychiatry, 2014, 71(12): 1381.
[20]
Yong-Ku, Kim,. The role of pro-inflammatory cytokines in neuroinflammation, neurogenesis and the neuroendocrine system in major depression. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2016, 64: 277–284.
[21]
Felger, J. C. Inflammatory cytokines in depression: Neurobiological mechanisms and therapeutic implications. Neuroscience, 2013, 246: 199–229.
[22]
Dantzer, R., O’Connor, J. C., Freund, G. G., Johnson, R. W., Kelley, K. W. From inflammation to sickness and depression: When the immune system subjugates the brain. Nature Reviews Neuroscience, 2008, 9(1): 46–56.
[23]
Angelopoulou, E., Piperi, C., Papavassiliou, A. G. High-mobility group box 1 in Parkinson’s disease: From pathogenesis to therapeutic approaches. Journal of Neurochemistry, 2018, 146(3): 211–218.
[24]
Musumeci, D., Roviello, G. N., Montesarchio, D. An overview on HMGB1 inhibitors as potential therapeutic agents in HMGB1-related pathologies. Pharmacology & Therapeutics, 2014, 141(3): 347–357.
[25]
Wen-Jun, Su,. Blocking the trigger: An integrative view on the anti-inflammatory therapy of depression. Brain, Behavior, and Immunity, 2019, 82: 10–12.
[26]
Goodwin, G. H., Johns, E. W. Isolation and characterisation of two calf-thymus chromatin non-histone proteins with high contents of acidic and basic amino acids. European Journal of Biochemistry, 1973, 40(1): 215–219.
[27]
Merenmies, J., Pihlaskari, R., Laitinen, J., Wartiovaara, J., Rauvala, H. 30-kDa heparin-binding protein of brain (amphoterin) involved in neurite outgrowth. Amino acid sequence and localization in the filopodia of the advancing plasma membrane. Journal of Biological Chemistry, 1991, 266(25): 16722–16729.
[28]
Kang, R., Chen, R. C., Zhang, Q. H., Hou, W., Wu, S., Cao, L. Z., Huang, J., Yu, Y., Fan, X. G., Yan, Z. W. et al. HMGB1 in health and disease. Molecular Aspects of Medicine, 2014, 40: 1–116.
[29]
Lotze, M. T., Tracey, K. J. High-mobility group box 1 protein (HMGB1): Nuclear weapon in the immune arsenal. Nature Reviews Immunology, 2005, 5(4): 331–342.
[30]
Wang, H. C., Bloom, O., Zhang, M. H., Vishnubhakat, J. M., Ombrellino, M., Che, J. T., Frazier, A., Yang, H., Ivanova, S., Borovikova, L. et al. HMG-1 as a late mediator of endotoxin lethality in mice. Science, 1999, 285(5425): 248–251.
[31]
Wang, H., Yang, H., Tracey, K. J. Extracellular role of HMGB1 in inflammation and sepsis. Journal of Internal Medicine, 2004, 255(3): 320–331.
[32]
RYBKA, J. P.2.g.001 HMGB1 and IL-17 are the mediators linking redox signalling and inflammation in depression. European Neuropsychopharmacology, 2013, 23: S414.
[33]
RYBKA, J., CATTANEO, A., KEDZIORA-KORNATOWSKA, K. P.4.037 HMGB1 signalling alters T-cell functioning in response to redox status in depressed patients: Effect on glucocorticoid receptor function. European Neuropsychopharmacology, 2013, 23: S98.
[34]
Rybka, J., Kedziora-Kornatowska, K., Kupczyk, D., Kedziora, J. 1944–HMGB1 danger signaling modulates t cells phenotype and cytokine profile in response to redox status in depressed patients. an effect on glucocorticoid receptor function. European Psychiatry, 2013, 28: 1.
[35]
Marie-Claire, C., Courtin, C., Curis, E., Bouaziz-Amar, E., Laplanche, J. L., Jacob, A., Etain, B., Blanchard, A., Bellivier, F. Increased plasma levels of high mobility group box 1 protein in patients with bipolar disorder: A pilot study. Journal of Neuroimmunology, 2019, 334: 576993.
[36]
Wang, S., Zhao, X. Y., Qiao, Z. W., Jia, X. D., Qi, Y. D. Paeoniflorin attenuates depressive behaviors in systemic lupus erythematosus mice. Biomedicine & Pharmacotherapy, 2018, 103: 248–252.
[37]
Oktayoglu, P., Tahtasiz, M., Bozkurt, M., Em, S., Ucar, D., Yazmalar, L., Mete, N., Nas, K., Gezer, O. Serum levels of high mobility group box 1 protein and its association with quality of life and psychological and functional status in patients with fibromyalgia. International Journal of Rheumatic Diseases, 2013, 16(4): 403–407.
[38]
Wu, T. Y., Liu, L., Zhang, W., Zhang, Y., Liu, Y. Z., Shen, X. L., Gong, H., Yang, Y. Y., Bi, X. Y., Jiang, C. L. et al. High-mobility group box-1 was released actively and involved in LPS induced depressive-like behavior. Journal of Psychiatric Research, 2015, 64: 99–106.
[39]
Yang, F., Zhu, W., Cai, X., Zhang, W., Yu, Z., Li, X. Minocycline alleviates NLRP3 inflammasome-dependent pyroptosis in monosodium glutamate-induced depressive rats. Biochemical and Biophysical Research Communications, 2020, 526(3): 553–559.
[40]
Fu, H. L., Liu, L., Tong, Y., Li, Y. J., Zhang, X., Gao, X. J., Yong, J. J., Zhao, J. J., Xiao, D., Wen, K. S. et al. The antidepressant effects of hesperidin on chronic unpredictable mild stress-induced mice. European Journal of Pharmacology, 2019, 853: 236–246.
[41]
Liu, L. M., Zhao, Z. X., Lu, L. W., Liu, J. Q., Sun, J., Dong, J. C. Icariin and icaritin ameliorated hippocampus neuroinflammation via mediating HMGB1 expression in social defeat model in mice. International Immunopharmacology, 2019, 75: 105799.
[42]
Tang, Y. T., Zhao, X., Antoine, D., Xiao, X. Z., Wang, H. C., Andersson, U., Billiar, T. R., Tracey, K. J., Lu, B. Regulation of posttranslational modifications of HMGB1 during immune responses. Antioxidants & Redox Signaling, 2016, 24(12): 620–634.
[43]
Cao, S. R., Li, S., Wang, Y. T., Shen, J. N., Zhou, Y., Li, H. Y., Yu, X. Q., Mao, H. P. Acetylation of HMGB1 by JNK1 signaling promotes LPS-induced peritoneal mesothelial cells apoptosis. BioMed Research International, 2018, 2018: 1–12.
[44]
Kim, Y. M., Park, E. J., Kim, J. H., Park, S. W., Kim, H. J., Chang, K. C. Ethyl pyruvate inhibits the acetylation and release of HMGB1 via effects on SIRT1/STAT signaling in LPS-activated RAW264.7 cells and peritoneal macrophages. International Immunopharmacology, 2016, 41: 98–105.
[45]
Lu, B., Antoine, D. J., Kwan, K., Lundbäck, P., Wähämaa, H., Schierbeck, H., Robinson, M., Van Zoelen, M. A., Yang, H., Li, J. et al. JAK/STAT1 signaling promotes HMGB1 hyperacetylation and nuclear translocation. Proceedings of the National Academy of Sciences of the United States of America, 2014, 111(8): 3068–3073.
[46]
Vogel, S., Bodenstein, R., Chen, Q. W., Feil, S., Feil, R., Rheinlaender, J., Schäffer, T. E., Bohn, E., Frick, J. S., Borst, O. et al. Platelet-derived HMGB1 is a critical mediator of thrombosis. Journal of Clinical Investigation, 2015, 125(12): 4638–4654.
[47]
Andersson, U., Yang, H., Harris, H. Extracellular HMGB1 as a therapeutic target in inflammatory diseases. Expert Opinion on Therapeutic Targets, 2018, 22(3): 263–277.
[48]
Kim, S. J., Ryu, M. J., Han, J., Jang, Y., Lee, M. J., Ju, X. S., Ryu, I., Lee, Y. L., Oh, E., Chung, W. et al. Non-cell autonomous modulation of tyrosine hydroxylase by HMGB1 released from astrocytes in an acute MPTP-induced Parkinsonian mouse model. Laboratory Investigation, 2019, 99(9): 1389–1399.
[49]
Su, J., Pan, Y. W., Wang, S. Q., Li, X. Z., Huang, F., Ma, S. P. Saikosaponin-d attenuated lipopolysaccharide-induced depressive-like behaviors via inhibiting microglia activation and neuroinflammation. International Immunopharmacology, 2020, 80: 106181.
[50]
Yang, H., Wang, H. C., Andersson, U. Targeting inflammation driven by HMGB1. Frontiers in Immunology, 2020, 11: 484.
[51]
Hisaoka-Nakashima, K., Azuma, H., Ishikawa, F., Nakamura, Y., Wang, D. L., Liu, K. Y., Wake, H., Nishibori, M., Nakata, Y., Morioka, N. Corticosterone induces HMGB1 release in primary cultured rat cortical astrocytes: Involvement of pannexin-1 and P2X7 receptor-dependent mechanisms. Cells, 2020, 9(5): 1068.
[52]
Abdulmahdi, W., Patel, D., Rabadi, M. M., Azar, T., Jules, E., Lipphardt, M., Hashemiyoon, R., Ratliff, B. B. HMGB1 redox during sepsis. Redox Biology, 2017, 13: 600–607.
[53]
Andersson, U., Antoine, D. J., Tracey, K. J. Expression of Concern: The functions of HMGB1 depend on molecular localization and post-translational modifications. Journal of Internal Medicine, 2014, 276(5): 420–424.
[54]
Paudel, Y. N., Angelopoulou, E., Piperi, C., Balasubramaniam, V. R. M. T., Othman, I., Shaikh, M. F. Enlightening the role of high mobility group box 1 (HMGB1) in inflammation: Updates on receptor signalling. European Journal of Pharmacology, 2019, 858: 172487.
[55]
Lian, Y. J., Gong, H., Wu, T. Y., Su, W. J., Zhang, Y., Yang, Y. Y., Peng, W., Zhang, T., et al. Ds-HMGB1 and fr-HMGB induce depressive behavior through neuroinflammation in contrast to nonoxid-HMGB1. Brain, Behavior, and Immunity, 2017, 59: 322–332.
[56]
Wang, B., Lian, yong‑jie, Su, wen‑jun, Liu, lin‑lin, Li, jia‑mei, Jiang, chun‑lei, Wang, yun‑xia. Fr‑HMGB1 and ds‑HMGB1 activate the kynurenine pathway via different mechanisms in association with depressive‑like behavior. Molecular Medicine Reports, 2019: 359–367.
[57]
Wang, B., Lian, Y. J., Dong, X., Peng, W., Liu, L. L., Su, W. J., Gong, H., Zhang, T., et al. Glycyrrhizic acid ameliorates the kynurenine pathway in association with its antidepressant effect. Behavioural Brain Research, 2018, 353: 250–257.
[58]
Wang, B., Lian, Y. J., Su, W. J., Peng, W., Dong, X., Liu, L. L., Gong, H., Zhang, T., et al. HMGB1 mediates depressive behavior induced by chronic stress through activating the kynurenine pathway. Brain, Behavior, and Immunity, 2018, 72: 51–60.
[59]
Bianchi, M. E., Crippa, M. P., Manfredi, A. A., Mezzapelle, R., Rovere Querini, P., Venereau, E. High-mobility group box 1 protein orchestrates responses to tissue damage via inflammation, innate and adaptive immunity, and tissue repair. Immunological Reviews, 2017, 280(1): 74–82.
[60]
Parkkinen, J., Raulo, E., Merenmies, J., Nolo, R., Kajander, E. O., Baumann, M., Rauvala, H. Amphoterin, the 30-kDa protein in a family of HMG1-type polypeptides. Enhanced expression in transformed cells, leading edge localization, and interactions with plasminogen activation. Journal of Biological Chemistry, 1993, 268(26): 19726–19738.
[61]
Andersson, U, Yang, H, Harris, H. High-mobility group box 1 protein (HMGB1) operates as an alarmin outside as well as inside cells. Seminars in Immunology, 2018, 38: 40–48.
[62]
LeBlanc, P. M., Doggett, T. A., Choi, J., Hancock, M. A., Durocher, Y., Frank, F., Nagar, B., Ferguson, T. A., Saleh, M. An immunogenic peptide in the A-box of HMGB1 protein reverses apoptosis-induced tolerance through RAGE receptor. The Journal of Biological Chemistry, 2014, 289(11): 7777–7786.
[63]
Hori, O., Brett, J., Slattery, T., Cao, R., Zhang, J. H., Chen, jing xian, Nagashima, M., Lundh, E. R., Vijay, S., Nitecki, D. et al. The receptor for advanced glycation end products (RAGE) is a cellular binding site for amphoterin. Journal of Biological Chemistry, 1995, 270(43): 25752–25761.
[64]
Huebener, P., Pradere, J. P., Hernandez, C., Gwak, G. Y., Caviglia, J. M., Mu, X. R., Loike, J. D., Schwabe, R. F. The HMGB1/RAGE axis triggers neutrophil-mediated injury amplification following necrosis. The Journal of Clinical Investigation, 2015, 125(2): 539–550.
[65]
Kokkola, R., Andersson, Mullins, G., Östberg, T., Treutiger, C. J., Arnold, B., Nawroth, P., Andersson, U., Harris, R. A., Harris, H. E. RAGE is the major receptor for the proinflammatory activity of HMGB1 in rodent macrophages. Scandinavian Journal of Immunology, 2005, 61(1): 1–9.
[66]
Sims, G. P., Rowe, D. C., Rietdijk, S. T., Herbst, R., Coyle, A. J. HMGB1 and RAGE in inflammation and cancer. Annual Review of Immunology, 2010, 28: 367–388.
[67]
Bopp, C., Bierhaus, A., Hofer, S., Bouchon, A., Nawroth, P. P., Martin, E., Weigand, M. A. Bench- to-bedside review: The inflammation-perpetuating pattern-recognition receptor RAGE as a therapeutic target in sepsis. Critical Care (London, England), 2008, 12(1): 201.
[68]
Pranal, T., Pereira, B., Berthelin, P., Roszyk, L., Godet, T., Chabanne, R., Eisenmann, N., Lautrette, A., Belville, C., Blondonnet, R. et al. Clinical and biological predictors of plasma levels of soluble RAGE in critically ill patients: Secondary analysis of a prospective multicenter observational study. Disease Markers, 2018, 2018: 1–13.
[69]
Colhoun, H. M., Betteridge, D. J., Durrington, P., Hitman, G., Neil, A., Livingstone, S., Charlton-Menys, V., Bao, W. H., Demicco, D. A., Preston, G. M. et al. Total soluble and endogenous secretory receptor for advanced glycation end products as predictive biomarkers of coronary heart disease risk in patients with type 2 diabetes: An analysis from the CARDS trial. Diabetes, 2011, 60(9): 2379–2385.
[70]
Franklin, T. C., Wohleb, E. S., Zhang, Y., Fogaça, M., Hare, B., Duman, R. S. Persistent increase in microglial RAGE contributes to chronic stress-induced priming of depressive-like behavior. Biological Psychiatry, 2018, 83(1): 50–60.
[71]
García Bueno, B., Caso, J. R., Madrigal, J. L., Leza, J. C. Innate immune receptor Toll-like receptor 4 signalling in neuropsychiatric diseases. Neuroscience & Biobehavioral Reviews, 2016, 64: 134–147.
[72]
Kawai, T., Akira, S. Antiviral signaling through pattern recognition receptors. The Journal of Biochemistry, 2007, 141(2): 137–145.
[73]
Liu, J. J., Buisman-Pijlman, F., Hutchinson, M. R. Toll-like receptor 4: Innate immune regulator of neuroimmune and neuroendocrine interactions in stress and major depressive disorder. Frontiers in Neuroscience, 2014, 8: 309.
[74]
Rahimifard, M., Maqbool, F., Moeini-Nodeh, S., Niaz, K., Abdollahi, M., Braidy, N., Nabavi, S. M., Nabavi, S. F. Targeting the TLR4 signaling pathway by polyphenols: A novel therapeutic strategy for neuroinflammation. Ageing Research Reviews, 2017, 36: 11–19.
[75]
KéRI, S, SZABó, C, Kelemen, O. Expression of Toll-Like Receptors in peripheral blood mononuclear cells and response to cognitive-behavioral therapy in major depressive disorder. Brain, Behavior, and Immunity, 2014, 40: 235–243.
[76]
Pandey, G. N., Rizavi, H. S., Ren, X. G., Bhaumik, R., Dwivedi, Y. Toll-like receptors in the depressed and suicide brain. Journal of Psychiatric Research, 2014, 53: 62–68.
[77]
Hung, Y. Y., Wu, M. K., Tsai, M. C., Huang, Y. L., Kang, H. Y. Aberrant expression of intracellular let-7e, miR-146a, and miR-155 correlates with severity of depression in patients with major depressive disorder and is ameliorated after antidepressant treatment. Cells, 2019, 8(7): E647.
[78]
Cheng, Y., Pardo, M., Armini, R. S., Martinez, A., Mouhsine, H., Zagury, J. F., Jope, R. S., Beurel, E. Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior. Brain, Behavior, and Immunity, 2016, 53: 207–222.
[79]
Yang, H., Wang, H., Ju, Z., Ragab, A. A., Lundbäck, P., Long, W., Valdes-Ferrer, S. I., He, M., Pribis, J. P., Li, J. et al. MD-2 is required for disulfide HMGB1-dependent TLR4 signaling. The Journal of Experimental Medicine, 2015, 212(1): 5–14.
[80]
Huising, M. O., Stet, R. J., Kruiswijk, C. P., Savelkoul, H. F., Lidy Verburg-van Kemenade, B. M. Molecular evolution of CXC chemokines: Extant CXC chemokines originate from the CNS. Trends in Immunology, 2003, 24(6): 306–312.
[81]
Bajetto, A., Bonavia, R., Barbero, S., Florio, T., Schettini, G. Chemokines and their receptors in the central nervous system. Frontiers in Neuroendocrinology, 2001, 22(3): 147–184.
[82]
Ma, Q., Jones, D., Borghesani, P. R., Segal, R. A., Nagasawa, T., Kishimoto, T., Bronson, R. T., Springer, T. A. Impaired B-lymphopoiesis, myelopoiesis, and derailed cerebellar neuron migration in CXCR4- and SDF-1-deficient mice. Proceedings of the National Academy of Sciences of the United States of America, 1998, 95(16): 9448–9453.
[83]
Yang, L., Wang, M., Guo, Y. Y., Sun, T., Li, Y. J., Yang, Q., Zhang, K., Liu, S. B., et al. Systemic inflammation induces anxiety disorder through CXCL12/CXCR4 pathway. Brain, Behavior, and Immunity, 2016, 56: 352–362.
[84]
de Filippo, K., Rankin, S. M. CXCR4, the master regulator of neutrophil trafficking in homeostasis and disease. European Journal of Clinical Investigation, 2018, 48(Suppl Suppl 2): e12949.
[85]
Ewa, A., Ogłodek,. Comparison of chemokines (CCL-5 and SDF-1), chemokine receptors (CCR-5 and CXCR-4) and IL-6 levels in patients with different severities of depression. Pharmacological Reports, 2014, 66(5): 920–926.
[86]
Madison, J. M., Zhou, F., Nigam, A., Hussain, A., Barker, D. D., Nehme, R., van der Ven, K., Hsu, J., Wolf, P., Fleishman, M. et al. Characterization of bipolar disorder patient-specific induced pluripotent stem cells from a family reveals neurodevelopmental and mRNA expression abnormalities. Molecular Psychiatry, 2015, 20(6): 703–717.
[87]
Heinisch, S., Kirby, L. G. SDF-1α/CXCL12 enhances GABA and glutamate synaptic activity at serotonin neurons in the rat dorsal raphe nucleus. Neuropharmacology, 2010, 58(2): 501–514.
[88]
Trojan, E., Ślusarczyk, J., Chamera, K., Kotarska, K., Głombik, K., Kubera, M., Basta-Kaim, A. The modulatory properties of chronic antidepressant drugs treatment on the brain chemokine–chemokine receptor network: A molecular study in an animal model of depression. Frontiers in Pharmacology, 2017, 8: 779.
[89]
Barbosa, I. G., Rocha, N. P., Vieira, E. L., Camkurt, M. A., Huguet, R. B., Guimarães, F. T. L., de Brito-Melo, G. E., Mendonça, V. A., Bauer, M. E., Teixeira, A. L. Decreased percentage of CD4+ lymphocytes expressing chemokine receptors in bipolar disorder. Acta Neuropsychiatrica, 2019, 31(5): 246–251.
[90]
Schiraldi, M., Raucci, A., Muñoz, L. M., Livoti, E., Celona, B., Venereau, E., Apuzzo, T., De Marchis, F., Pedotti, M., Bachi, A. et al. HMGB1 promotes recruitment of inflammatory cells to damaged tissues by forming a complex with CXCL12 and signaling via CXCR4. The Journal of Experimental Medicine, 2012, 209(3): 551–563.
[91]
Zhan, L. Y., Lei, S. Q., Zhang, B. H., Li, W. L., Wang, H. X., Zhao, B., Cui, S. S., Ding, H., Huang, Q. M. Overexpression of miR-381 relieves neuropathic pain development via targeting HMGB1 and CXCR4. Biomedicine & Pharmacotherapy, 2018, 107: 818–823.
[92]
Kohler, O., Krogh, J., Mors, O., Eriksen Benros, M. Inflammation in depression and the potential for anti-inflammatory treatment. Current Neuropharmacology, 2016, 14(7): 732–742.
[93]
Mollica, L., De Marchis, F., Spitaleri, A., Dallacosta, C., Pennacchini, D., Zamai, M., Agresti, A., Trisciuoglio, L., et al. Glycyrrhizin binds to high-mobility group box 1 protein and inhibits its cytokine activities. Chemistry & Biology, 2007, 14(4): 431–441.
[94]
Cao, Z. Y., Liu, Y. Z., Li, J. M., Ruan, Y. M., Yan, W. J., Zhong, S. Y., Zhang, T., Liu, L. L.. et al. Glycyrrhizic acid as an adjunctive treatment for depression through anti-inflammation: A randomized placebo-controlled clinical trial. Journal of Affective Disorders, 2020, 265: 247–254.
[95]
Guo, Z. G., Zhao, F., Wang, Y., Wang, Y., Geng, M. M., Zhang, Y. L., Ma, Q. X., Xu, X. Z. Sevoflurane exerts an anti-depressive action by blocking the HMGB1/TLR4 pathway in unpredictable chronic mild stress rats. Journal of Molecular Neuroscience, 2019, 69(4): 546–556.
[96]
Liu, L., Dong, Y., Shan, X., Li, L., Xia, B., Wang, H. Anti-depressive effectiveness of baicalin in vitro and in vivo. Molecules, 2019, 24(2): E326.
[97]
Liu, L., Zhao, Z., Lu, L., Liu, J., Sun, J., Wu, X., Dong, J. Icariin and icaritin ameliorated hippocampus neuroinflammation via inhibiting HMGB1-related pro-inflammatory signals in lipopolysaccharide-induced inflammation model in C57BL/6 J mice. International Immunopharmacology, 2019, 68: 95–105.
[98]
Hisaoka-Nakashima, K., Tomimura, Y., Yoshii, T., Ohata, K., Takada, N., Zhang, F. F., Nakamura, Y., Liu, K. Y., Wake, H., Nishibori, M. et al. High-mobility group box 1-mediated microglial activation induces anxiodepressive-like behaviors in mice with neuropathic pain. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 2019, 92: 347–362.
[99]
Miller, A. H. Beyond depression: The expanding role of inflammation in psychiatric disorders. World Psychiatry, 2020, 19(1): 108–109.
[100]
Fries, G. R., Saldana, V. A., Finnstein, J., Rein, T. Molecular pathways of major depressive disorder converge on the synapse. Molecular Psychiatry, 2023, 28(1): 284–297.
Stress and Brain
Pages 109-122
Cite this article:
Jiang Q, Li C, Xu H, et al. Inflammatory signaling of HMGB1 in depressive disorder. Stress and Brain, 2023, 3(3): 109-122. https://doi.org/10.26599/SAB.2023.9060001

593

Views

52

Downloads

0

Crossref

Altmetrics

Received: 14 September 2023
Revised: 07 November 2023
Accepted: 10 November 2023
Published: 05 November 2023
© The Author(s) 2023

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attributtion-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission.

Return