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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Respir+Res
2017 ; 18
(1
): 172
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Anti-fibrotic efficacy of nintedanib in pulmonary fibrosis via the inhibition of
fibrocyte activity
#MMPMID28915889
Sato S
; Shinohara S
; Hayashi S
; Morizumi S
; Abe S
; Okazaki H
; Chen Y
; Goto H
; Aono Y
; Ogawa H
; Koyama K
; Nishimura H
; Kawano H
; Toyoda Y
; Uehara H
; Nishioka Y
Respir Res
2017[Sep]; 18
(1
): 172
PMID28915889
show ga
BACKGROUND: Nintedanib, a tyrosine kinase inhibitor that is specific for
platelet-derived growth factor receptors (PDGFR), fibroblast growth factor
receptors (FGFR), and vascular endothelial growth factor receptors (VEGFR), has
recently been approved for idiopathic pulmonary fibrosis. Fibrocytes are bone
marrow-derived progenitor cells that produce growth factors and contribute to
fibrogenesis in the lungs. However, the effects of nintedanib on the functions of
fibrocytes remain unclear. METHODS: Human monocytes were isolated from the
peripheral blood of healthy volunteers. The expression of growth factors and
their receptors in fibrocytes was analyzed using ELISA and Western blotting. The
effects of nintedanib on the ability of fibrocytes to stimulate lung fibroblasts
were examined in terms of their proliferation. The direct effects of nintedanib
on the differentiation and migration of fibrocytes were also assessed. We
investigated whether nintedanib affected the accumulation of fibrocytes in mouse
lungs treated with bleomycin. RESULTS: Human fibrocytes produced PDGF, FGF2, and
VEGF-A. Nintedanib and specific inhibitors for each growth factor receptor
significantly inhibited the proliferation of lung fibroblasts stimulated by the
supernatant of fibrocytes. Nintedanib inhibited the migration and differentiation
of fibrocytes induced by growth factors in vitro. The number of fibrocytes in the
bleomycin-induced lung fibrosis model was reduced by the administration of
nintedanib, and this was associated with anti-fibrotic effects. CONCLUSIONS:
These results support the role of fibrocytes as producers of and responders to
growth factors, and suggest that the anti-fibrotic effects of nintedanib are at
least partly mediated by suppression of fibrocyte function.
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