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Genistein does not inhibit TGF-beta1-induced conversion of human dermal fibroblasts to myofibroblasts

Publikace na 1. lékařská fakulta, 3. lékařská fakulta |
2021

Tento text není v aktuálním jazyce dostupný. Zobrazuje se verze "en".Abstrakt

Transforming growth factor beta 1 (TGF-beta1) is a pro-fibrotic cytokine with a key role in wound repair and regeneration, including induction of fibroblast-to-myofibroblast transition. Genistein is a naturally occurring selective estrogen receptor modulator with promising anti-fibrotic properties.

In the present study we aimed to investigate whether genistein modulates TGF-beta1 (canonical and non-canonical) signaling in normal dermal fibroblasts at the protein level (Western blot and immunofluorescence). We demonstrated that TGF-beta1 induces the myofibroblast-like phenotype in the studied fibroblast signaling via canonical (SMAD) and non-canonical (AKT, ERK1/2, ROCK) pathways.

Genistein induced only ERK1/2 expression, whereas the combination of TGF-beta1 and genistein attenuated the ERK1/2 and ROCK signaling. Of note, the other studied pathways remained almost unaffected.

From this point of view, genistein does not impair conversion of normal fibroblasts to myofibroblast-like cells.