Livin upregulation in keratinocytes of psoriasis patients to promote adhesion molecule expression

Activation of keratinocytes (KCs) is the main pathological feature of psoriasis. KCs recruit neutrophils by releasing various antimicrobial peptides and chemokines, which is also related to the expression of KC adhesion molecules. However, the regulatory mechanism governing their expression is still unclear. Livin, an inhibitor of the apoptosis protein family member involved in proliferation and metastasis of tumor cells, is significantly increased in psoriatic lesions.

[1]  Miri Kim,et al.  Angiogenesis in Chronic Inflammatory Skin Disorders , 2021, International journal of molecular sciences.

[2]  Ho-Cheol Kang,et al.  Inhibitor of apoptosis protein Livin promotes tumor progression and chemoradioresistance in human anaplastic thyroid cancer. , 2021, Oncology reports.

[3]  A. Trevani,et al.  Protein A Modulates Neutrophil and Keratinocyte Signaling and Survival in Response to Staphylococcus aureus , 2021, Frontiers in Immunology.

[4]  A. Waisman,et al.  Imiquimod-Induced Psoriasis in Mice Depends on the IL-17 Signaling of Keratinocytes. , 2019, The Journal of investigative dermatology.

[5]  J. Gudjonsson,et al.  Neutrophil Extracellular Traps Promote Inflammatory Responses in Psoriasis via Activating Epidermal TLR4/IL-36R Crosstalk , 2019, Front. Immunol..

[6]  Gang Wang,et al.  Neutrophil exosomes enhance the skin autoinflammation in generalized pustular psoriasis via activating keratinocytes , 2019, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[7]  H. Katayama Development of psoriasis by continuous neutrophil infiltration into the epidermis , 2018, Experimental dermatology.

[8]  Chi-Yuan Chen,et al.  Topical application of anthranilate derivatives ameliorates psoriatic inflammation in a mouse model by inhibiting keratinocyte‐derived chemokine expression and neutrophil infiltration , 2018, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[9]  X. Wang,et al.  The inhibitor of apoptosis protein livin is upregulated in psoriasis vulgaris , 2018, Journal of the European Academy of Dermatology and Venereology : JEADV.

[10]  K. Schäkel,et al.  RNA-antimicrobial peptide complexes fuel a TLR- and NETosis-mediated inflammatory cycle of neutrophil activation in psoriasis , 2018, bioRxiv.

[11]  G. Núñez,et al.  Staphylococcus aureus Virulent PSMα Peptides Induce Keratinocyte Alarmin Release to Orchestrate IL-17-Dependent Skin Inflammation. , 2017, Cell host & microbe.

[12]  Leping Li,et al.  Livin serves as a prognostic marker for mid-distal rectal cancer and a target of mid-distal rectal cancer treatment , 2017, Oncology letters.

[13]  M. Migliario,et al.  Low concentrations of neutrophil extracellular traps induce proliferation in human keratinocytes via NF-kB activation. , 2017, Journal of dermatological science.

[14]  T. Mayadas,et al.  Lactoferrin Suppresses Neutrophil Extracellular Traps Release in Inflammation , 2016, EBioMedicine.

[15]  N. Borregaard,et al.  Neutrophil extracellular traps - the dark side of neutrophils. , 2016, The Journal of clinical investigation.

[16]  A. Yang,et al.  Effects of monomethoxypolyethylene glycol-chitosan nanoparticle-mediated dual silencing of livin and survivin genes in prostate cancer PC-3M cells. , 2016, Genetics and molecular research : GMR.

[17]  Q. Lu,et al.  The Inflammatory Response in Psoriasis: a Comprehensive Review , 2016, Clinical Reviews in Allergy & Immunology.

[18]  Seamus J. Martin,et al.  Neutrophil-Derived Proteases Escalate Inflammation through Activation of IL-36 Family Cytokines. , 2016, Cell reports.

[19]  Y. Joo,et al.  Livin is associated with the invasive and oncogenic phenotypes of human hepatocellular carcinoma cells , 2015, Hepatology research : the official journal of the Japan Society of Hepatology.

[20]  F. Bernard,et al.  Inhibition of Keratinocyte Differentiation by the Synergistic Effect of IL-17A, IL-22, IL-1α, TNFα and Oncostatin M , 2014, PloS one.

[21]  C. Allis,et al.  Histone hypercitrullination mediates chromatin decondensation and neutrophil extracellular trap formation , 2009, The Journal of cell biology.

[22]  Mei Han,et al.  Challenge and promise: roles for Livin in progression and therapy of cancer , 2008, Molecular Cancer Therapeutics.

[23]  Jongdae Lee,et al.  IAP Suppression of Apoptosis Involves Distinct Mechanisms: the TAK1/JNK1 Signaling Cascade and Caspase Inhibition , 2002, Molecular and Cellular Biology.

[24]  Xie-wan Chen,et al.  Clinical benefits of Livin peptide-loaded DCs/CIKs combined with chemotherapy in advanced non-small cell lung cancer. , 2019, American journal of cancer research.