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Inhibition of fibrocyte differentiation by serum amyloid P
#MMPMID14607961
Pilling D
; Buckley CD
; Salmon M
; Gomer RH
J Immunol
2003[Nov]; 171
(10
): 5537-46
PMID14607961
show ga
Wound healing and the dysregulated events leading to fibrosis both involve the
proliferation and differentiation of fibroblasts and the deposition of
extracellular matrix. Whether these fibroblasts are locally derived or from a
circulating precursor population is unclear. Fibrocytes are a distinct population
of fibroblast-like cells derived from peripheral blood monocytes that enter sites
of tissue injury to promote angiogenesis and wound healing. We have found that
CD14(+) peripheral blood monocytes cultured in the absence of serum or plasma
differentiate into fibrocytes within 72 h. We purified the factor in serum and
plasma that prevents the rapid appearance of fibrocytes, and identified it as
serum amyloid P (SAP). Purified SAP inhibits fibrocyte differentiation at levels
similar to those found in plasma, while depleting SAP reduces the ability of
plasma to inhibit fibrocyte differentiation. Compared with sera from healthy
individuals and patients with rheumatoid arthritis, sera from patients with
scleroderma and mixed connective tissue disease, two systemic fibrotic diseases,
were less able to inhibit fibrocyte differentiation in vitro and had
correspondingly lower serum levels of SAP. These results suggest that low levels
of SAP may thus augment pathological processes leading to fibrosis. These data
also suggest mechanisms to inhibit fibrosis in chronic inflammatory conditions,
or conversely to promote wound healing.
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