Erratum to MMP28 promotes macrophage polarization toward M2 cells and augments pulmonary fibrosis (Journal of Leukocyte Biology, (2014), 10.1189/jlb.1112587);MMP28 promotes macrophage polarization toward M2 cells and augments pulmonary fibrosis

Journal of Leukocyte Biology

Volumn 95, Issue 1, 2014, Pages 9-18

  Gharib, Sina A ^a   Johnston, Laura K ^a   Huizar, Isham ^b   Birkland, Timothy P ^a   Hanson, Josiah ^a   Wang, Ying ^a   Parks, William C ^a   Manicone, Anne M ^a  

^a UNIVERSITY OF WASHINGTON   (United States)

^b TEXAS TECH UNIVERSITY HEALTH SCIENCES CENTER   (United States)

Author keywords

Epilysin; Inflammation; M1; Monocytes

Indexed keywords

BLEOMYCIN; COLLAGEN; GELATINASE A; INTERLEUKIN 13; INTERLEUKIN 4; LIPOPOLYSACCHARIDE; MATRIX METALLOPROTEINASE 28; UNCLASSIFIED DRUG; CYTOKINE; MATRIX METALLOPROTEINASE; MMP28 PROTEIN, HUMAN; TOLL LIKE RECEPTOR;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BLEOMYCIN-INDUCED PULMONARY FIBROSIS; CONTROLLED STUDY; GENE EXPRESSION; IN VITRO STUDY; IN VIVO STUDY; LUNG FIBROSIS; LUNG INJURY; MACROPHAGE; MACROPHAGE FUNCTION; MOUSE; NONHUMAN; PHENOTYPE; POLARIZATION; PRIORITY JOURNAL; PSEUDOMONAS AERUGINOSA; WEIGHT REDUCTION; WILD TYPE; ANIMAL; APOPTOSIS; BONE MARROW CELL; CELL DIFFERENTIATION; CYTOLOGY; DISEASE MODEL; DRUG ANTAGONISM; DRUG EFFECT; EPILYSIN; GENE EXPRESSION PROFILING; GENE EXPRESSION REGULATION; GENE REGULATORY NETWORK; GENETICS; IMMUNOLOGY; INFLAMMATION; KNOCKOUT MOUSE; LUNG ALVEOLUS MACROPHAGE; METABOLISM; MONOCYTE; PHYSIOLOGICAL STRESS; SIGNAL TRANSDUCTION;

EPILYSIN; INFLAMMATION; MONOCYTES;

ANIMALS; APOPTOSIS; BONE MARROW CELLS; CELL DIFFERENTIATION; CYTOKINES; DISEASE MODELS, ANIMAL; GENE EXPRESSION; GENE EXPRESSION PROFILING; GENE EXPRESSION REGULATION; GENE REGULATORY NETWORKS; INFLAMMATION; MACROPHAGES; MACROPHAGES, ALVEOLAR; MATRIX METALLOPROTEINASES, SECRETED; MICE; MICE, KNOCKOUT; MONOCYTES; PULMONARY FIBROSIS; SIGNAL TRANSDUCTION; STRESS, PHYSIOLOGICAL; TOLL-LIKE RECEPTORS;

EID: 84897019330     PISSN: 07415400     EISSN: 19383673     Source Type: Journal    
DOI: 10.1189/jlb.1112587.err     Document Type: Erratum

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