Impact of high‐mobility group box 1 on melanocytic survival and its involvement in the pathogenesis of vitiligo

Vitiligo is attributable to loss of functional melanocytes and is the most common acquired depigmenting disorder. Oxidative stress and intense ultraviolet irradiation are known to aggravate this condition. The nonhistone high‐mobility group box 1 (HMGB1) DNA‐binding protein is a physiological activator of immune responses, cellular proliferation and cell death. Although it is implicated in the pathogenesis of autoimmune diseases and cutaneous disorders, the precise role of HMGB1 in melanocytes has yet to be studied.

[1]  Jonathan C. Fuller,et al.  The HMGB1 protein induces a metabolic type of tumour cell death by blocking aerobic respiration , 2016, Nature Communications.

[2]  I. Joosten,et al.  High mobility group box 1 is increased in the sera of psoriatic patients with disease progression , 2016, Journal of the European Academy of Dermatology and Venereology : JEADV.

[3]  Mingxian Chen,et al.  HMGB1 induces apoptosis and EMT in association with increased autophagy following H/R injury in cardiomyocytes , 2016, International journal of molecular medicine.

[4]  S. J. Han,et al.  HMGB1 in the pathogenesis of ultraviolet-induced ocular surface inflammation , 2015, Cell Death and Disease.

[5]  Marisa Ponpuak,et al.  Secretory autophagy. , 2015, Current opinion in cell biology.

[6]  P. Song,et al.  Impaired activation of the Nrf2-ARE signaling pathway undermines H2O2-induced oxidative stress response: a possible mechanism for melanocyte degeneration in vitiligo. , 2014, The Journal of investigative dermatology.

[7]  Jeon-Soo Shin,et al.  The Role of High Mobility Group Box 1 in Innate Immunity , 2014, Yonsei medical journal.

[8]  Ji Young Kim,et al.  Protease-activated receptor-2 activates NQO-1 via Nrf2 stabilization in keratinocytes. , 2014, Journal of dermatological science.

[9]  Victoria Barygina,et al.  SIRT1 regulates MAPK pathways in vitiligo skin: insight into the molecular pathways of cell survival , 2014, Journal of cellular and molecular medicine.

[10]  T. Oberyszyn,et al.  Ultraviolet light exposure stimulates HMGB1 release by keratinocytes , 2013, Archives of Dermatological Research.

[11]  A. Sodhi,et al.  Ultraviolet B induces high mobility group box 1 release from mouse peritoneal macrophages in vitro via caspase-1 mediated secretion pathway. , 2013, Immunobiology.

[12]  J. Ortonne,et al.  Activation of the unfolded protein response in vitiligo: the missing link? , 2012, The Journal of investigative dermatology.

[13]  Ai-Young Lee.  Role of Keratinocytes in the Development of Vitiligo , 2012, Annals of dermatology.

[14]  S. Amin,et al.  Autophagosomal Membrane Serves as Platform for Intracellular Death-inducing Signaling Complex (iDISC)-mediated Caspase-8 Activation and Apoptosis* , 2012, The Journal of Biological Chemistry.

[15]  U. Andersson,et al.  HMGB1: A multifunctional alarmin driving autoimmune and inflammatory disease , 2012, Nature Reviews Rheumatology.

[16]  D. Parsad,et al.  Melanocytorrhagy and apoptosis in vitiligo: connecting jigsaw pieces. , 2012, Indian journal of dermatology, venereology and leprology.

[17]  Annamaria Vezzani,et al.  High-mobility group box-1 impairs memory in mice through both toll-like receptor 4 and Receptor for Advanced Glycation End Products , 2011, Experimental Neurology.

[18]  C. Kallenberg,et al.  High mobility group box 1 (HMGB1) and anti-HMGB1 antibodies and their relation to disease characteristics in systemic lupus erythematosus , 2011, Arthritis research & therapy.

[19]  K. Tracey,et al.  HMGB1 is a therapeutic target for sterile inflammation and infection. , 2011, Annual review of immunology.

[20]  Guy S. Salvesen,et al.  SnapShot: Caspases , 2011, Cell.

[21]  Jason P. Zlotnicki,et al.  High Mobility Group Box 1 Release from Hepatocytes during Ischemia and Reperfusion Injury Is Mediated by Decreased Histone Deacetylase Activity* , 2010, The Journal of Biological Chemistry.

[22]  Frank O. Nestle,et al.  Skin immune sentinels in health and disease , 2009, Nature Reviews Immunology.

[23]  B. Burlando,et al.  HMGb1 promotes scratch wound closure of HaCaT keratinocytes via ERK1/2 activation , 2009, Molecular and Cellular Biochemistry.

[24]  D. Bani,et al.  Keratinocyte dysfunction in vitiligo epidermis: cytokine microenvironment and correlation to keratinocyte apoptosis. , 2009, Histology and histopathology.

[25]  G. Kroemer,et al.  Autophagic cell death: the story of a misnomer , 2008, Nature Reviews Molecular Cell Biology.

[26]  M. Zeegers,et al.  Vitiligo pathogenesis: autoimmune disease, genetic defect, excessive reactive oxygen species, calcium imbalance, or what else? , 2008, Experimental dermatology.

[27]  H. Harris,et al.  Translocation of the novel cytokine HMGB1 to the cytoplasm and extracellular space coincides with the peak of clinical activity in experimentally UV-induced lesions of cutaneous lupus erythematosus , 2007, Lupus.

[28]  Haichao Wang,et al.  Hydrogen peroxide stimulates macrophages and monocytes to actively release HMGB1 , 2007, Journal of leukocyte biology.

[29]  R. Paus,et al.  Towards the development of a simplified long‐term organ culture method for human scalp skin and its appendages under serum‐free conditions , 2007, Experimental dermatology.

[30]  D. Pisetsky,et al.  The extracellular release of HMGB1 during apoptotic cell death. , 2006, American journal of physiology. Cell physiology.

[31]  Jong-sang Park,et al.  HMGB1, a Novel Cytokine-Like Mediator Linking Acute Neuronal Death and Delayed Neuroinflammation in the Postischemic Brain , 2006, The Journal of Neuroscience.

[32]  E. Wagner,et al.  Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins , 2005, Nature.

[33]  C. Enerbäck,et al.  Psoriasin (S100A7) and calgranulin-B (S100A9) induction is dependent on reactive oxygen species and is downregulated by Bcl-2 and antioxidants , 2005, Cancer biology & therapy.

[34]  Eric H. Baehrecke,et al.  Autophagy: dual roles in life and death? , 2005, Nature Reviews Molecular Cell Biology.

[35]  R. Deberardinis,et al.  Autophagy in metazoans: cell survival in the land of plenty , 2005, Nature Reviews Molecular Cell Biology.

[36]  Kevin J. Tracey,et al.  High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal , 2005, Nature Reviews Immunology.

[37]  Takeshi Tokuhisa,et al.  The role of autophagy during the early neonatal starvation period , 2004, Nature.

[38]  F. Scheiflinger,et al.  Native Versus Recombinant High-Mobility Group B1 Proteins: Functional Activity In Vitro , 2004, Inflammation.

[39]  R. Boissy,et al.  On the etiology of contact/occupational vitiligo. , 2004, Pigment cell research.

[40]  U. Andersson,et al.  Mini‐review: The nuclear protein HMGB1 as a proinflammatory mediator , 2004, European journal of immunology.

[41]  G. Imokawa.  Autocrine and paracrine regulation of melanocytes in human skin and in pigmentary disorders. , 2004, Pigment cell research.

[42]  E. Dvoryankova,et al.  Modern Aspects of Vitiligo Pathogenesis , 2004, Doklady Biological Sciences.

[43]  M. Yamakuchi,et al.  High mobility group box chromosomal protein 1 plays a role in the pathogenesis of rheumatoid arthritis as a novel cytokine. , 2003, Arthritis and rheumatism.

[44]  T. Misteli,et al.  Release of chromatin protein HMGB1 by necrotic cells triggers inflammation , 2002, Nature.

[45]  H. Rokos,et al.  Oxidative stress in vitiligo: photo-oxidation of pterins produces H(2)O(2) and pterin-6-carboxylic acid. , 2002, Biochemical and biophysical research communications.

[46]  W. Westerhof,et al.  Expression and modulation of apoptosis regulatory molecules in human melanocytes: significance in vitiligo , 2000, The British journal of dermatology.

[47]  C. Jahoda.  Cellular and developmental aspects of androgenetic alopecia , 1998, Experimental dermatology.

[48]  Y. Lazebnik,et al.  Caspases: enemies within. , 1998, Science.

[49]  R. Moll,et al.  Characterization of epidermal wound healing in a human skin organ culture model: acceleration by transplanted keratinocytes. , 1998, The Journal of investigative dermatology.

[50]  S. Passi,et al.  Epidermal oxidative stress in vitiligo. , 1998, Pigment cell research.

[51]  J. Kieffer,et al.  Inflammatory skin disease in transgenic mice that express high levels of interleukin 1 alpha in basal epidermis. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[52]  L. Packer,et al.  Enzymic and non-enzymic antioxidants in epidermis and dermis of human skin. , 1994, The Journal of investigative dermatology.

[53]  E. Maytin.  Differential effects of heat shock and UVB light upon stress protein expression in epidermal keratinocytes. , 1992, The Journal of biological chemistry.