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The pro-fibrotic properties of transforming growth factor on human fibroblasts
are counteracted by caffeic acid by inhibiting myofibroblast formation and
collagen synthesis
#MMPMID26453399
Mia MM
; Bank RA
Cell Tissue Res
2016[Mar]; 363
(3
): 775-89
PMID26453399
show ga
Fibrosis is a chronic disorder affecting many organs. A universal process in
fibrosis is the formation of myofibroblasts and the subsequent collagen
deposition by these cells. Transforming growth factor beta1 (TGF?1) plays a major
role in the formation of myofibroblasts, e.g. by activating fibroblasts.
Currently, no treatments are available to circumvent fibrosis. Caffeic acid
phenethyl ester (CAPE) shows a broad spectrum of biological activities, including
anti-fibrotic properties in vivo in mice and rats. However, little is known about
the direct effects of CAPE on fibroblasts. We have tested whether CAPE is able to
suppress myofibroblast formation and collagen formation of human dermal and lung
fibroblasts exposed to TGF?1, and found that this was indeed the case. In fact,
the formation of myofibroblasts by TGF?1 and subsequent collagen formation was
completely abolished by CAPE. The same was observed for fibronectin and tenascin
C. The lack of myofibroblast formation is likely due to the suppression of GLI1
and GLI2 expression by CAPE because of diminished nuclear SMAD2/3 levels.
Post-treatment with CAPE after myofibroblast formation even resulted in a partial
reversal of myofibroblasts into fibroblasts and/or reduction in collagen
formation. Major discrepancies were seen between mRNA levels of collagen type I
and cells stained positive for collagen, underlining the need for protein data in
fibrosis studies to make reliable conclusions.
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