Placental extract suppresses the formation of fibrotic deposits by tumor necrosis factor alpha and transforming growth factor beta-induced epithelial–mesenchymal transition in ARPE-19 cells

Epithelial-mesenchymal transition (EMT) is involved in the development of proliferative vitreoretinopathy (PVR) and subsequent fibrosis. Previously, we demonstrated that placental extract ameliorates fibrosis in a mouse model of non-alcoholic steatohepatitis. In this study, we evaluated whether plac...

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Bibliographic Details
Published in:BMC research notes 2021-11, Vol.14 (1), p.1-407, Article 407
Main Authors: Igarashi, Kyoko, Sugimoto, Koji, Hirano, Eiichi
Format: Article
Language:English
Subjects:
ARPE-19
Bioactivity
Care and treatment
Cell differentiation
Cytokines
Epithelial cells
Epithelial–mesenchymal transition
Extracellular matrix
Fatty liver
Fibrosis
Gene expression
Growth factors
Health aspects
Medical research
Medicine, Experimental
Mesenchyme
Necrosis
Pathogenesis
Physiological aspects
Placenta
Placental extract
Proliferative vitreoretinopathy
Research Note
Retinal detachment
Retinal pigment epithelium
Stem cells
Tissue extracts
Transforming growth factor-b
Transforming growth factors
Tumor necrosis factor
Tumor necrosis factor-TNF
Tumor necrosis factor-α
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Summary:Epithelial-mesenchymal transition (EMT) is involved in the development of proliferative vitreoretinopathy (PVR) and subsequent fibrosis. Previously, we demonstrated that placental extract ameliorates fibrosis in a mouse model of non-alcoholic steatohepatitis. In this study, we evaluated whether placental extract influences EMT and fibrosis through cytokine-induced EMT in the retinal pigment epithelial cells, in vitro. Placental extract did not inhibit EMT, but it suppressed excessive mesenchymal reactions and the subsequent fibrosis. These results suggest that placental extract effectively ameliorates EMT-associated fibrosis in PVR. This beneficial effect could be partially attributed to the suppression of excessive mesenchymal reactions.
ISSN:1756-0500
1756-0500
DOI:10.1186/s13104-021-05824-0