Genistein does not Inhibit TGF-β1-Induced Conversion of Human Dermal Fibroblasts to Myofibroblasts

Transforming growth factor beta 1 (TGF-β1) 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...

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Bibliographic Details
Published in:Physiological research 2021-10, Vol.70 (5), p.815-820
Main Authors: KAŇUCHOVÁ, M, URBAN, L, MELEGOVÁ, N, ČOMA, M, DVOŘÁNKOVÁ, B, SMETANA, K, GÁL, P
Format: Article
Language:English
Subjects:
AKT protein
Antibodies
Cytokines
Estrogen receptors
Estrogens
Fibroblasts
Genistein
Growth factors
Immunofluorescence
Kinases
Phenotypes
Proteins
Short Communication
Signal transduction
Smad protein
Transforming growth factor-b1
Wound healing
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Summary:Transforming growth factor beta 1 (TGF-β1) 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-β1 (canonical and non-canonical) signaling in normal dermal fibroblasts at the protein level (Western blot and immunofluo-rescence). We demonstrated that TGF-β1 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-β1 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.
ISSN:0862-8408
1802-9973
DOI:10.33549/physiolres.934666