TLR2, TLR4 and the Myd88 signaling pathway are crucial for neutrophil migration in acute kidney injury induced by sepsis

PLoS ONE

Volumn 7, Issue 5, 2012, Pages

  Castoldi, Angela ^a,b   Braga, Tárcio Teodoro ^b   Correa Costa, Matheus ^b   Aguiar, Cristhiane Fávero ^a   Bassi, Ênio José ^b   Correa Silva, Reinaldo ^a   Elias, Rosa Maria ^a   Salvador, Fábia ^a   Moraes Vieira, Pedro Manoel ^b   Cenedeze, Marcos Antônio ^a   Reis, Marlene Antônia ^d   Hiyane, Meire Ioshie ^b   Pacheco Silva, Álvaro ^a,c   Gonçalves, Giselle Martins ^b   Câmara, Niels Olsen Saraiva ^a,b  

^a FEDERAL UNIVERSITY OF SÃO PAULO   (Brazil)

^b UNIVERSITY OF SÃO PAULO   (Brazil)

^c HOSPITAL ISRAELITA ALBERT EINSTEIN   (Brazil)

^d FEDERAL UNIVERSITY OF TRIÂNGULO MINEIRO   (Brazil)

Author keywords

[No Author keywords available]

Indexed keywords

CYTOKINE; MYELOID DIFFERENTIATION FACTOR 88; TOLL LIKE RECEPTOR 2; TOLL LIKE RECEPTOR 4; TLR2 PROTEIN, MOUSE; TLR4 PROTEIN, MOUSE;

ACUTE KIDNEY FAILURE; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; BLOOD VESSEL PERMEABILITY; CELL INFILTRATION; CELL LOSS; CELL MIGRATION; CONTROLLED STUDY; CYTOKINE PRODUCTION; DISEASE EXACERBATION; ENZYME INHIBITION; HYPOXIA; INNATE IMMUNITY; INTRACELLULAR SIGNALING; KIDNEY FUNCTION; KIDNEY TUBULE CELL; KNOCKOUT MOUSE; MALE; MOUSE; NEPHRITIS; NEUTROPHIL; NONHUMAN; PERITONEAL CAVITY; PROTEIN EXPRESSION; PROTEIN FUNCTION; PROTEIN LOCALIZATION; RENAL PROTECTION; SEPSIS; WILD TYPE; ANIMAL; C57BL MOUSE; GENE DELETION; GENETICS; IMMUNOLOGY; KIDNEY; METABOLISM; MOUSE MUTANT; NEUTROPHIL CHEMOTAXIS; PATHOLOGY; SIGNAL TRANSDUCTION;

MUS;

ACUTE KIDNEY INJURY; ANIMALS; CYTOKINES; GENE DELETION; KIDNEY; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MYELOID DIFFERENTIATION FACTOR 88; NEUTROPHIL INFILTRATION; NEUTROPHILS; SEPSIS; SIGNAL TRANSDUCTION; TOLL-LIKE RECEPTOR 2; TOLL-LIKE RECEPTOR 4;

EID: 84861409518     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0037584     Document Type: Article

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