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[PMID]:28976190
[Au] Autor:Cunden LS; Brophy MB; Rodriguez GE; Flaxman HA; Nolan EM
[Ad] Endereço:Department of Chemistry, Massachusetts Institute of Technology , Cambridge, Massachusetts 02139, United States.
[Ti] Título:Biochemical and Functional Evaluation of the Intramolecular Disulfide Bonds in the Zinc-Chelating Antimicrobial Protein Human S100A7 (Psoriasin).
[So] Source:Biochemistry;56(43):5726-5738, 2017 Oct 31.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human S100A7 (psoriasin) is a metal-chelating protein expressed by epithelial cells. It is a 22-kDa homodimer with two EF-hand domains per subunit and two transition-metal-binding His Asp sites at the dimer interface. Each subunit contains two cysteine residues that can exist as free thiols (S100A7 ) or as an intramolecular disulfide bond (S100A7 ). Herein, we examine the disulfide bond redox behavior, the Zn(II) binding properties, and the antibacterial activity of S100A7, as well as the effect of Ca(II) ions on these properties. In agreement with prior work [Hein, K. Z., et al. (2013) Proc. Natl. Acad. Sci. U. S. A. 112, 13039-13044], we show that apo S100A7 is a substrate for the mammalian thioredoxin system; however, negligible reduction of the disulfide bond is observed for Ca(II)- and Zn(II)-bound S100A7 . Furthermore, metal binding depresses the midpoint potential of the disulfide bond. S100A7 and S100A7 each coordinate 2 equiv of Zn(II) with subnanomolar affinity in the absence and presence of Ca(II) ions, and the cysteine thiolates in S100A7 do not form a third high-affinity Zn(II) site. These results refute a prior model implicating the Cys thiolates of S100A7 in high-affinity Zn(II) binding [Hein, K. Z., et al. (2013) Proc. Natl. Acad. Sci. U. S. A. 112, 13039-13044]. S100A7 and the disulfide-null variants show comparable Zn(II)-depletion profiles; however, only S100A7 exhibits antibacterial activity against select bacterial species. Metal substitution experiments suggest that the disulfide bonds in S100A7 may enhance metal sequestration by the His Asp sites and thereby confer growth inhibitory properties to S100A7 .
[Mh] Termos MeSH primário: Antibacterianos/química
Quelantes/química
Dissulfetos/química
Multimerização Proteica
Proteínas S100/química
Zinco/química
[Mh] Termos MeSH secundário: Antibacterianos/metabolismo
Quelantes/metabolismo
Seres Humanos
Ligação Proteica
Proteína A7 Ligante de Cálcio S100
Proteínas S100/genética
Proteínas S100/metabolismo
Zinco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Chelating Agents); 0 (Disulfides); 0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100A7 protein, human); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00781


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[PMID]:28436180
[Au] Autor:Isobe N
[Ad] Endereço:Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima, Japan.
[Ti] Título:Control mechanisms for producing antimicrobial factors in ruminant mammary gland.
[So] Source:Anim Sci J;88(7):937-943, 2017 Jul.
[Is] ISSN:1740-0929
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Mastitis, a symptom of inflammation in mammary tissue by infection with various kinds of bacteria, causes huge economic losses in the milk industry. One of the popular methods for treatment of mastitis is antibiotics, although this prohibits milk shipping and sometimes causes resistant microbes. Therefore, a new strategy to treat mastitis without antibiotics is eagerly required around the world. Antimicrobial factors belong to innate immunity and can start their function extremely early after bacterial stimulation. These factors have antimicrobial activity for a broad spectrum of bacteria. Elucidation of causal mechanisms and functions of antimicrobial factors in the mammary gland is thought to result in suitable methods for prevention and treatment of mastitis. Therefore, this review introduces traits of some antimicrobial factors and the mechanisms for expressing, producing and secreting them in the mammary gland. For antimicrobial factors, lingual antimicrobial peptide (LAP), S100A7, cathelicidin and lactoferrin are controlled in different sites and different time courses, suggesting that antimicrobial factors play different roles for local defense against bacterial infection in the mammary gland. These findings will contribute to the development of prevention and treatment methods for mastitis.
[Mh] Termos MeSH primário: Peptídeos Catiônicos Antimicrobianos/imunologia
Lactoferrina/imunologia
Glândulas Mamárias Humanas/imunologia
Glândulas Mamárias Humanas/microbiologia
Mastite Bovina/prevenção & controle
Mastite Bovina/terapia
Proteínas S100/imunologia
beta-Defensinas/imunologia
[Mh] Termos MeSH secundário: Animais
Peptídeos Catiônicos Antimicrobianos/fisiologia
Bovinos
Feminino
Seres Humanos
Lactoferrina/fisiologia
Glândulas Mamárias Humanas/metabolismo
Mastite Bovina/imunologia
Mastite Bovina/microbiologia
Proteína A7 Ligante de Cálcio S100
Proteínas S100/fisiologia
beta-Defensinas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antimicrobial Cationic Peptides); 0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100A7 protein, human); 0 (beta-Defensins); 0 (lingual antimicrobial peptide); 143108-26-3 (CAP18 lipopolysaccharide-binding protein); EC 3.4.21.- (Lactoferrin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE
[do] DOI:10.1111/asj.12808


  3 / 237 MEDLINE  
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[PMID]:28422993
[Au] Autor:Zwicker S; Hattinger E; Bureik D; Batycka-Baran A; Schmidt A; Gerber PA; Rothenfusser S; Gilliet M; Ruzicka T; Wolf R
[Ad] Endereço:Department of Dermatology and Allergology, Ludwig-Maximilian University Munich, Frauenlobstr. 9-11, Munich, Germany.
[Ti] Título:Th17 micro-milieu regulates NLRP1-dependent caspase-5 activity in skin autoinflammation.
[So] Source:PLoS One;12(4):e0175153, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-1ß is a potent player in cutaneous inflammation and central for the development of a Th17 micro-milieu in autoinflammatory diseases including psoriasis. Its production is controlled at the transcriptional level and by subsequent posttranslational processing via inflammatory caspases. In this study, we detected inflammatory caspase-5 active in epidermal keratinocytes and in psoriatic skin lesions. Further, interferon-γ and interleukin-17A synergistically induced caspase-5 expression in cultured keratinocytes, which was dependent on the antimicrobial peptide psoriasin (S100A7). However, diseases-relevant triggers for caspase-5 activity and IL-1ß production remain unknown. Recently, extranuclear DNA has been identified as danger-signals abundant in the psoriatic epidermis. Here, we could demonstrate that cytosolic double-stranded (ds) DNA transfected into keratinocytes triggered the activation of caspase-5 and the release of IL-1ß. Further, interleukin-17A promoted caspase-5 function via facilitation of the NLRP1-inflammasome. Anti-inflammatory vitamin D interfered with the IL-1ß release and suppressed caspase-5 in keratinocytes and in psoriatic skin lesions. Our data link the disease-intrinsic danger signals psoriasin (S100A7) and dsDNA for NLPR1-dependent caspase-5 activity in psoriasis providing potential therapeutic targets in Th17-mediated skin autoinflammation.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Reguladoras de Apoptose/genética
Caspases/genética
Interleucina-17/genética
Interleucina-1beta/genética
Psoríase/genética
Pele/imunologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/imunologia
Proteínas Reguladoras de Apoptose/imunologia
Caspases/imunologia
Células Cultivadas
DNA/genética
DNA/imunologia
Regulação da Expressão Gênica
Seres Humanos
Inflamassomos/efeitos dos fármacos
Inflamassomos/imunologia
Interferon gama/farmacologia
Interleucina-17/antagonistas & inibidores
Interleucina-17/imunologia
Interleucina-17/farmacologia
Interleucina-1beta/imunologia
Interleucina-1beta/secreção
Queratinócitos/citologia
Queratinócitos/efeitos dos fármacos
Queratinócitos/imunologia
Psoríase/imunologia
Psoríase/patologia
Proteína A7 Ligante de Cálcio S100
Proteínas S100/genética
Proteínas S100/imunologia
Transdução de Sinais
Pele/patologia
Células Th17/efeitos dos fármacos
Células Th17/imunologia
Células Th17/patologia
Transfecção
Vitamina D/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Apoptosis Regulatory Proteins); 0 (IL17A protein, human); 0 (IL1B protein, human); 0 (Inflammasomes); 0 (Interleukin-17); 0 (Interleukin-1beta); 0 (NLRP1 protein, human); 0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100A7 protein, human); 1406-16-2 (Vitamin D); 82115-62-6 (Interferon-gamma); 9007-49-2 (DNA); EC 3.4.22.- (CASP5 protein, human); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0175153


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[PMID]:28393239
[Au] Autor:Liu Y; Bunston C; Hodson N; Resaul J; Sun PH; Cai S; Chen G; Gu Y; Satherley LK; Bosanquet DC; Al-Sarireh B; Tian X; Hao C; Jiang WG; Ye L
[Ad] Endereço:Metastasis and Angiogenesis Research Group, Cardiff China Medical Research Collaborative, Division of Cancer and Genetics, Cardiff University School of Medicine, Cardiff, CF14 4XN, UK.
[Ti] Título:Psoriasin promotes invasion, aggregation and survival of pancreatic cancer cells; association with disease progression.
[So] Source:Int J Oncol;50(5):1491-1500, 2017 May.
[Is] ISSN:1791-2423
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Psoriasin (S100A7) is an 11-kDa small calcium binding protein initially isolated from psoriatic skin lesions. It belongs to the S100 family of proteins which play an important role in a range of cell functions including proliferation, differentiation, migration and apoptosis. Aberrant Psoriasin expression has been implicated in a range of cancers and is often associated with poor prognosis. This study examined the role of Psoriasin on pancreatic cancer cell functions and the implication in progression of the disease. Expression of Psoriasin was determined in a cohort of pancreatic tissues comprised of 126 pancreatic tumours and 114 adjacent non-tumour pancreatic tissues. Knockdown and overexpression of Psoriasin in pancreatic cancer cells was performed using specifically constructed plasmids, which either had anti-Psoriasin ribozyme transgene or the full length human Psoriasin coding sequence. Psoriasin knockdown and overexpression was verified using conventional RT-PCR and qPCR. The effect of manipulating Psoriasin expression on pancreatic cancer cell functions was assessed using several in vitro cell function assays. Local invasive pancreatic cancers extended beyond the pancreas expressed higher levels of Psoriasin transcripts compared with the cancers confined to the pancreas. Primary tumours with distant metastases exhibited a reduced expression of Psoriasin. Psoriasin overexpression cell lines exhibited significantly increased growth and migration compared to control cells. In addition, Psoriasin overexpression resulted in increased pancreatic cancer cell invasion which was associated with upregulation of matrix metalloproteinase-2 (MMP-2) and MMP-9. Overexpression of Psoriasin also promoted aggregation and survival of pancreatic cancer cells when they lost anchorage. Taken together, higher expression of Psoriasin was associated with local invasion in pancreatic cancers. Psoriasin expression is associated with pancreatic cancer cell growth, migration, cell-matrix adhesion, and invasion via regulation of MMPs. As such, the proposed implications of Psoriasin in invasion, disease progression and as a potential therapeutic target warrant further investigation.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Agregação Celular/genética
Invasividade Neoplásica/genética
Neoplasias Pancreáticas/genética
Proteínas S100/genética
[Mh] Termos MeSH secundário: Apoptose/genética
Biomarcadores Tumorais/biossíntese
Movimento Celular/genética
Sobrevivência Celular/genética
Progressão da Doença
Feminino
Regulação Neoplásica da Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
Masculino
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 9 da Matriz/genética
Invasividade Neoplásica/patologia
Metástase Neoplásica
Neoplasias Pancreáticas/patologia
Proteína A7 Ligante de Cálcio S100
Proteínas S100/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100A7 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.3892/ijo.2017.3953


  5 / 237 MEDLINE  
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[PMID]:28333758
[Au] Autor:Plichta JK; Holmes CJ; Nienhouse V; Puszynski M; Gao X; Dong Q; Lin H; Sinacore J; Zilliox M; Toh E; Nelson DE; Gamelli RL; Radek KA
[Ad] Endereço:1Burn and Shock Trauma Research Institute, Loyola University Chicago, Health Sciences Campus, Maywood, IL. 2Department of Surgery, Loyola University Chicago, Health Sciences Campus, Maywood, IL. 3Department of Public Health Sciences, Stritch School of Medicine, Loyola University Chicago, Health Sciences Campus, Maywood, IL. 4Center for Biomedical Informatics, Loyola University Chicago, Health Sciences Campus, Maywood, IL. 5Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN.
[Ti] Título:Cutaneous Burn Injury Modulates Urinary Antimicrobial Peptide Responses and the Urinary Microbiome.
[So] Source:Crit Care Med;45(6):e543-e551, 2017 Jun.
[Is] ISSN:1530-0293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Characterization of urinary bacterial microbiome and antimicrobial peptides after burn injury to identify potential mechanisms leading to urinary tract infections and associated morbidities in burn patients. DESIGN: Retrospective cohort study using human urine from control and burn subjects. SETTING: University research laboratory. PATIENTS: Burn patients. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Urine samples from catheterized burn patients were collected hourly for up to 40 hours. Control urine was collected from "healthy" volunteers. The urinary bacterial microbiome and antimicrobial peptide levels and activity were compared with patient outcomes. We observed a significant increase in urinary microbial diversity in burn patients versus controls, which positively correlated with a larger percent burn and with the development of urinary tract infection and sepsis postadmission, regardless of age or gender. Urinary psoriasin and ß-defensin antimicrobial peptide levels were significantly reduced in burn patients at 1 and 40 hours postadmission. We observed a shift in antimicrobial peptide hydrophobicity and activity between control and burn patients when urinary fractions were tested against Escherichia coli and Enterococcus faecalis urinary tract infection isolates. Furthermore, the antimicrobial peptide activity in burn patients was more effective against E. coli than E. faecalis. Urinary tract infection-positive burn patients with altered urinary antimicrobial peptide activity developed either an E. faecalis or Pseudomonas aeruginosa urinary tract infection, suggesting a role for urinary antimicrobial peptides in susceptibility to select uropathogens. CONCLUSIONS: Our data reveal potential links for urinary tract infection development and several morbidities in burn patients through alterations in the urinary microbiome and antimicrobial peptides. Overall, this study supports the concept that early assessment of urinary antimicrobial peptide responses and the bacterial microbiome may be used to predict susceptibility to urinary tract infections and sepsis in burn patients.
[Mh] Termos MeSH primário: Queimaduras/epidemiologia
Queimaduras/urina
Microbiota/fisiologia
Urina/microbiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Peptídeos Catiônicos Antimicrobianos/urina
Enterococcus faecalis/isolamento & purificação
Ensaio de Imunoadsorção Enzimática
Escherichia coli/isolamento & purificação
Feminino
Seres Humanos
Masculino
Testes de Sensibilidade Microbiana
Meia-Idade
Pseudomonas aeruginosa/isolamento & purificação
Estudos Retrospectivos
Proteína A7 Ligante de Cálcio S100
Proteínas S100/urina
Fatores de Tempo
beta-Defensinas/urina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimicrobial Cationic Peptides); 0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100A7 protein, human); 0 (beta-Defensins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1097/CCM.0000000000002304


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[PMID]:28112393
[Au] Autor:Jansen S; Kress E; Fragoulis A; Wruck CJ; Wolf R; Grötzinger J; Michalek M; Pufe T; Tauber SC; Brandenburg LO
[Ad] Endereço:Department of Anatomy and Cell Biology, RWTH Aachen University, Aachen, Germany.
[Ti] Título:Psoriasin has divergent effects on the innate immune responses of murine glial cells.
[So] Source:J Neurochem;141(1):86-99, 2017 Apr.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Antimicrobial peptides are an important part of the innate immune defense in the central nervous system (CNS). The expression of the antimicrobial peptides psoriasin (S100A7) is up-regulated during bacterial meningitis. However, the exact mechanisms induced by psoriasin to modulate glial cell activity are not yet fully understood. Our hypothesis is that psoriasin induced pro- and anti-inflammatory signaling pathways as well as regenerative factors to contribute in total to a balanced immune response. Therefore, we used psoriasin-stimulated glial cells and analyzed the translocation of the pro-inflammatory transcription factor nuclear factor 'kappa-light-chain-enhancer' of activated B-cells (NFκB) in murine glial cells and the expression of pro- and anti-inflammatory mediators by real time RT-PCR, ELISA technique, and western blotting. Furthermore, the relationship between psoriasin and the antioxidative stress transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) was investigated. Stimulation with psoriasin not only enhanced NFκB translocation and increased the expression of the pro-inflammatory cytokines, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF- α) but also neurotrophin expression. Evidence for functional interactions between psoriasin and Nrf2 were detected in the form of increased antioxidant response element (ARE) activity and induction of Nrf2/ARE-dependent heme oxygenase 1 (HO-1) expression in psoriasin-treated microglia and astrocytes. The results illustrate the ability of psoriasin to induce immunological functions in glia cells where psoriasin exerts divergent effects on the innate immune response.
[Mh] Termos MeSH primário: Imunidade Inata/fisiologia
Neuroglia/imunologia
Neuroglia/metabolismo
Proteínas S100/imunologia
Proteínas S100/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Células Cultivadas
Feminino
Células HEK293
Seres Humanos
Imunidade Inata/efeitos dos fármacos
Mediadores da Inflamação/imunologia
Mediadores da Inflamação/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neuroglia/efeitos dos fármacos
Proteína A7 Ligante de Cálcio S100
Proteínas S100/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100a7a protein, mouse)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.13959


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[PMID]:28060905
[Au] Autor:Lei H; Li X; Jing B; Xu H; Wu Y
[Ad] Endereço:Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Chemical Biology Division of Shanghai Universities E-Institutes, Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medic
[Ti] Título:Human S100A7 Induces Mature Interleukin1α Expression by RAGE-p38 MAPK-Calpain1 Pathway in Psoriasis.
[So] Source:PLoS One;12(1):e0169788, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Psoriatic keratinocytes express exaggerated levels of inflammatory cytokines, and show aberrant hyperproliferation and terminal differentiation in the pathogenesis of psoriasis. The antimicrobial protein hS100A7 (psoriasin) has been found highly expressed in psoriatic skin, but the mechanism and physiological function remain largely unknown. We observed that hS100A7 induces mature interleukin 1α (17kDa) expression in normal human epidermal keratinocytes, which is dependent on RAGE-p38 MAPK and calpain-1 as the inhibitors or knockdown of them completely decreased the expression of mature interleukin1α. Then, we proved mS100a7a15, mature IL-1α and calpain-1 were highly expressed in imquimod-induced psoriasis model and mouse IL-17a-neutralizing antibody treatment attenuated mS100a7a15 expression. At last, PD 151746 (calpain-1 inhibitor) treatment decreased epidermal thickness in imquimod-induced psoriasis model. Taken together, our results suggest that mature IL-1α induced by hS100A7 is via RAGE-p38 MAPK and calpain-1 pathway in keratinocyte and this mechanism may play an important role during psoriasis.
[Mh] Termos MeSH primário: Calpaína/metabolismo
Interleucina-1alfa/metabolismo
Psoríase/metabolismo
Psoríase/patologia
Receptor para Produtos Finais de Glicação Avançada/metabolismo
Proteínas S100/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Acrilatos/farmacologia
Animais
Linhagem Celular
Modelos Animais de Doenças
Expressão Gênica
Seres Humanos
Hiperplasia
Interleucina-1alfa/genética
Queratinócitos/metabolismo
Camundongos
Proteólise
Psoríase/genética
Proteína A7 Ligante de Cálcio S100
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acrylates); 0 (Interleukin-1alpha); 0 (PD 151746); 0 (Receptor for Advanced Glycation End Products); 0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100A7 protein, human); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.4.22.- (Calpain); EC 3.4.22.52 (CAPNS1 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0169788


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[PMID]:27958610
[Au] Autor:Ekman AK; Vegfors J; Eding CB; Enerbäck C
[Ad] Endereço:Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Linköping University, SE-581 85 Linköping, Sweden.
[Ti] Título:Overexpression of Psoriasin (S100A7) Contributes to Dysregulated Differentiation in Psoriasis.
[So] Source:Acta Derm Venereol;97(4):441-448, 2017 Apr 06.
[Is] ISSN:1651-2057
[Cp] País de publicação:Sweden
[La] Idioma:eng
[Ab] Resumo:Psoriasin, which is highly expressed in psoriasis, is encoded by a gene located within the epidermal differentiation complex. The aim of this study was to investigate the effect of endogenous psoriasin on disturbed keratinocyte differentiation in psoriasis. Immunohistochemical staining revealed a gradient of psoriasin expression in the psoriatic epidermis with highest expression in the suprabasal, differentiated layers. Induction of keratinocyte differentiation caused concurrent expression of psoriasin and the differentiation marker involucrin. The differentiation-induced psoriasin expression was found to be mediated by the protein kinase C pathway. The downregulation of psoriasin expression by small interfering RNA revealed that psoriasin mediates the expression of involucrin, desmoglein 1, transglutaminase 1 and CD24 in normal differentiation. The lentivirus-mediated overexpression of psoriasin, mimicking the psoriatic milieu, gave rise to an altered regulation of differentiation genes and an expression pattern reminiscent of that in psoriatic epidermis. These findings suggest that psoriasin contributes to the dysregulated differentiation process in the psoriasis epidermis.
[Mh] Termos MeSH primário: Diferenciação Celular
Epiderme/metabolismo
Queratinócitos/metabolismo
Psoríase/metabolismo
Proteínas S100/metabolismo
[Mh] Termos MeSH secundário: Antígeno CD24/genética
Antígeno CD24/metabolismo
Estudos de Casos e Controles
Células Cultivadas
Desmogleína 1/genética
Desmogleína 1/metabolismo
Epiderme/patologia
Seres Humanos
Queratinócitos/patologia
Proteína Quinase C/metabolismo
Precursores de Proteínas/genética
Precursores de Proteínas/metabolismo
Psoríase/genética
Psoríase/patologia
Interferência de RNA
Proteína A7 Ligante de Cálcio S100
Proteínas S100/genética
Transdução de Sinais
Transfecção
Transglutaminases/genética
Transglutaminases/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD24 Antigen); 0 (CD24 protein, human); 0 (DSG1 protein, human); 0 (Desmoglein 1); 0 (Protein Precursors); 0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100A7 protein, human); 60108-77-2 (involucrin); EC 2.3.2.13 (Transglutaminases); EC 2.3.2.13 (transglutaminase 1); EC 2.7.11.13 (Protein Kinase C)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161214
[St] Status:MEDLINE
[do] DOI:10.2340/00015555-2596


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[PMID]:27535424
[Au] Autor:Lei H; Wang Y; Zhang T; Chang L; Wu Y; Lai Y
[Ad] Endereço:Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, 200241, China.
[Ti] Título:TLR3 activation induces S100A7 to regulate keratinocyte differentiation after skin injury.
[So] Source:Sci China Life Sci;60(2):158-167, 2017 Feb.
[Is] ISSN:1869-1889
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Human S100A7 (psoriasin) is highly expressed in psoriasis and other inflammatory diseases; however, the function of S100A7 in wound repair remains largely unknown. Here we demonstrated that skin injury increased the expression of S100A7. Damaged cells from wounded skin induced the expression of S100A7 via the activation of Toll-like receptor 3 (TLR3) followed by the activation of p38 MAPK. S100A7, in turn, acted on keratinocytes to induce the expression of terminal differentiation marker gene loricrin through the activation of p38 MAPK and caspase-1. The differentiation of keratinocytes induced by S100A7 resulted in skin stratification, thus efficiently promoting wound closure. Taken together, our results demonstrate that the activation of TLR3 accelerates wound closure via the induction of S100A7 to induce keratinocyte differentiation. These findings also provide new insights into the development of different forms of treatment with skin wounds.
[Mh] Termos MeSH primário: Diferenciação Celular
Queratinócitos/citologia
Proteínas S100/metabolismo
Pele/lesões
Receptor 3 Toll-Like/metabolismo
Cicatrização
[Mh] Termos MeSH secundário: Animais
Caspase 1/metabolismo
Células Cultivadas
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Poli I-C
Polinucleotídeos/farmacologia
Proteína A7 Ligante de Cálcio S100
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Polynucleotides); 0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100A7 protein, human); 0 (TLR3 protein, human); 0 (Toll-Like Receptor 3); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.4.22.36 (Caspase 1); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160819
[St] Status:MEDLINE
[do] DOI:10.1007/s11427-016-0027-2


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[PMID]:27996128
[Au] Autor:Mishra S; Ahirwar DK; Ganju RK
[Ad] Endereço:Department of Pathology, Ohio State University Medical Center, Columbus, OH, U.S.A.
[Ti] Título:Psoriasin (S100A7): a novel mediator of angiogenesis.
[So] Source:Br J Dermatol;175(6):1141-1142, 2016 Dec.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Neovascularização Patológica
Proteínas S100
[Mh] Termos MeSH secundário: Seres Humanos
Proteína A7 Ligante de Cálcio S100
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100A7 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.15141



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