Cellular origins of fibroblasts: Possible implications for organ fibrosis in systemic sclerosis

Current Opinion in Rheumatology

Volumn 16, Issue 6, 2004, Pages 733-738

  Postlethwaite, Arnold E ^a   Shigemitsu, Hidenobu ^a,b   Kanangat, Siva ^a,b  

^a UNIVERSITY OF TENNESSEE HEALTH SCIENCE CENTER   (United States)

^b VETERANS AFFAIRS MEDICAL CENTER   (United States)

Author keywords

Epithelial mesenchymal transition; Monocyte; Scleroderma; Transdifferentiation; Transition

Indexed keywords

AMYLOID PROTEIN; BONE MORPHOGENETIC PROTEIN; CD14 ANTIGEN; CYTOKINE; ISOPROTEIN; TRANSFORMING GROWTH FACTOR;

ANIMAL CELL; CELL CULTURE; CONCENTRATION (PARAMETERS); EMBRYO DEVELOPMENT; EPITHELIUM CELL; FIBROBLAST; FIBROSIS; HUMAN; KIDNEY FIBROSIS; LUPUS VULGARIS; MESENCHYME CELL; MONOCYTE; MOUSE; MYOFIBROBLAST; NONHUMAN; PERIPHERAL BLOOD MONONUCLEAR CELL; PLURIPOTENT STEM CELL; PRIORITY JOURNAL; REVIEW; RHEUMATIC DISEASE; SCLERODERMA; SERUM; SYSTEMIC SCLEROSIS;

FIBROBLASTS; FIBROSIS; HUMANS; SCLERODERMA, SYSTEMIC;

EID: 7044224913     PISSN: 10408711     EISSN: None     Source Type: Journal    
DOI: 10.1097/01.bor.0000139310.77347.9c     Document Type: Review

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30. 1. J Immunol 2003, 171:5537-5546. Excellent demonstration that serum amyloid protein inhibits fibrocyte development and that SSc sera have low levels of serum amyloid protein. These low levels are postulated to possibly predispose SSc monocytes to transdifferentiate into fibrocytes.