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Bone marrow-derived fibrocytes contribute to liver fibrosis
#MMPMID25966982
Xu J
; Kisseleva T
Exp Biol Med (Maywood)
2015[Jun]; 240
(6
): 691-700
PMID25966982
show ga
Chronic liver injury often leads to hepatic fibrosis, a condition associated with
increased levels of circulating TGF-?1 and lipopolysaccharide, activation of
myofibroblasts, and extensive deposition of extracellular matrix, mostly collagen
Type I. Hepatic stellate cells are considered to be the major(1) but not the only
source of myofibroblasts in the injured liver.(2) Hepatic myofibroblasts may also
originate from portal fibroblasts, mesenchymal cells, and fibrocytes.(3) Since
the discovery of fibrocytes in 1994 by Dr. Bucala and colleagues, this bone
marrow (BM)-derived collagen Type I-producing CD45(+) cells remain the most
fascinating cells of the hematopoietic system. Due to the ability to
differentiate into collagen Type I producing cells/myofibroblasts, fibrocytes
were implicated in the pathogenesis of liver, skin, lung, and kidney fibrosis.
However, studies of different organs often contain controversial results on the
number of fibrocytes recruited to the site of injury and their biological
function. Furthermore, fibrocytes were implicated in the pathogenesis of sepsis
and were shown to possess antimicrobial activity. Finally, in response to
specific stimuli, fibrocytes can give rise to fully differentiated macrophages,
suggesting that in concurrence with the high plasticity of hematopoietic cells,
fibrocytes exhibit progenitor properties. Here, we summarize our current
understanding of the role of CD45(+)Collagen Type I(+) BM-derived cells in
response to fibrogenic liver injury and septicemia and discuss the most recent
evidence supporting the critical role of fibrocytes in the mediation of
pro-fibrogenic and/or pro-inflammatory responses.
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