Molecular action of isoflavone genistein in the human epithelial cell line HaCaT

Due to its strong proliferation-reducing effects on keratinocytes, and also anti-inflammatory properties, the isoflavone genistein has already been proposed as a possible antipsoriatic compound. As there is still no detailed information on this topic, we examined the effects of genistein by using an...

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Vydané v:	PloS one Ročník 13; číslo 2; s. e0192297
Hlavní autori:	Smolińska, Elwira, Moskot, Marta, Jakóbkiewicz-Banecka, Joanna, Węgrzyn, Grzegorz, Banecki, Bogdan, Szczerkowska-Dobosz, Aneta, Purzycka-Bohdan, Dorota, Gabig-Cimińska, Magdalena
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States Public Library of Science 14.02.2018 Public Library of Science (PLoS)
Predmet:	1-Phosphatidylinositol 3-kinase Activation Analysis Anti-inflammatory agents Biochemistry Biology and Life Sciences Biophysics Cytotoxicity Dermatology Epithelial cells Experimental design Fibroblasts Gene expression Genes Genetic aspects Genetics Genistein Inflammation Interleukin 20 Interleukin 8 Isoflavones Keratinocytes Kinases Laboratories Lipopolysaccharides Medicine and Health Sciences Metabolism Molecular biology Monocyte chemoattractant protein 1 NF-κB protein Nuclear transport Physiological aspects Psoriasis Research and Analysis Methods Ribonucleic acid RNA Signaling Skin Skin diseases Transcription Translocation Tumor necrosis factor-α Poland United States > US Netherlands
ISSN:	1932-6203, 1932-6203
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Abstract	Due to its strong proliferation-reducing effects on keratinocytes, and also anti-inflammatory properties, the isoflavone genistein has already been proposed as a possible antipsoriatic compound. As there is still no detailed information on this topic, we examined the effects of genistein by using an in vitro model of both, normal and "psoriasis-like" keratinocytes at this stage of our work exhaustively testing the selected flavonoid in a mono-treated experimental design. Gene expression studies revealed transcriptional changes that confirms known disease-associated pathways and highlights many psoriasis-related genes. Our results suggested that aberrant expression of genes contributing to the progress of psoriasis could be improved by the action of genistein. Genistein prevented "cytokine mix" as well as TNF-α-induced NF-κB nuclear translocation, with no effect on the PI3K signaling cascade, indicating the luck of turning this pathway into NF-κB activation. It could have attenuated TNF-α and LPS-induced inflammatory responses by suppressing ROS activation. Regardless of the type of keratinocyte stimulation used, reduction of cytokine IL-8, IL-20 and CCL2 production (both at RNA and protein level) following genistein treatment was visible. Because investigations of other groups supported our commentary on potential administration of genistein as a potential weapon in the armamentarium against psoriasis, it is believed that this paper should serve to encourage researchers to conduct further studies on this subject.
AbstractList	Due to its strong proliferation-reducing effects on keratinocytes, and also anti-inflammatory properties, the isoflavone genistein has already been proposed as a possible antipsoriatic compound. As there is still no detailed information on this topic, we examined the effects of genistein by using an in vitro model of both, normal and "psoriasis-like" keratinocytes at this stage of our work exhaustively testing the selected flavonoid in a mono-treated experimental design. Gene expression studies revealed transcriptional changes that confirms known disease-associated pathways and highlights many psoriasis-related genes. Our results suggested that aberrant expression of genes contributing to the progress of psoriasis could be improved by the action of genistein. Genistein prevented "cytokine mix" as well as TNF-α-induced NF-κB nuclear translocation, with no effect on the PI3K signaling cascade, indicating the luck of turning this pathway into NF-κB activation. It could have attenuated TNF-α and LPS-induced inflammatory responses by suppressing ROS activation. Regardless of the type of keratinocyte stimulation used, reduction of cytokine IL-8, IL-20 and CCL2 production (both at RNA and protein level) following genistein treatment was visible. Because investigations of other groups supported our commentary on potential administration of genistein as a potential weapon in the armamentarium against psoriasis, it is believed that this paper should serve to encourage researchers to conduct further studies on this subject. Due to its strong proliferation-reducing effects on keratinocytes, and also anti-inflammatory properties, the isoflavone genistein has already been proposed as a possible antipsoriatic compound. As there is still no detailed information on this topic, we examined the effects of genistein by using an in vitro model of both, normal and "psoriasis-like" keratinocytes at this stage of our work exhaustively testing the selected flavonoid in a mono-treated experimental design. Gene expression studies revealed transcriptional changes that confirms known disease-associated pathways and highlights many psoriasis-related genes. Our results suggested that aberrant expression of genes contributing to the progress of psoriasis could be improved by the action of genistein. Genistein prevented "cytokine mix" as well as TNF-[alpha]-induced NF-[kappa]B nuclear translocation, with no effect on the PI3K signaling cascade, indicating the luck of turning this pathway into NF-[kappa]B activation. It could have attenuated TNF-[alpha] and LPS-induced inflammatory responses by suppressing ROS activation. Regardless of the type of keratinocyte stimulation used, reduction of cytokine IL-8, IL-20 and CCL2 production (both at RNA and protein level) following genistein treatment was visible. Because investigations of other groups supported our commentary on potential administration of genistein as a potential weapon in the armamentarium against psoriasis, it is believed that this paper should serve to encourage researchers to conduct further studies on this subject. Due to its strong proliferation-reducing effects on keratinocytes, and also anti-inflammatory properties, the isoflavone genistein has already been proposed as a possible antipsoriatic compound. As there is still no detailed information on this topic, we examined the effects of genistein by using an in vitro model of both, normal and "psoriasis-like" keratinocytes at this stage of our work exhaustively testing the selected flavonoid in a mono-treated experimental design. Gene expression studies revealed transcriptional changes that confirms known disease-associated pathways and highlights many psoriasis-related genes. Our results suggested that aberrant expression of genes contributing to the progress of psoriasis could be improved by the action of genistein. Genistein prevented "cytokine mix" as well as TNF-α-induced NF-κB nuclear translocation, with no effect on the PI3K signaling cascade, indicating the luck of turning this pathway into NF-κB activation. It could have attenuated TNF-α and LPS-induced inflammatory responses by suppressing ROS activation. Regardless of the type of keratinocyte stimulation used, reduction of cytokine IL-8, IL-20 and CCL2 production (both at RNA and protein level) following genistein treatment was visible. Because investigations of other groups supported our commentary on potential administration of genistein as a potential weapon in the armamentarium against psoriasis, it is believed that this paper should serve to encourage researchers to conduct further studies on this subject.Due to its strong proliferation-reducing effects on keratinocytes, and also anti-inflammatory properties, the isoflavone genistein has already been proposed as a possible antipsoriatic compound. As there is still no detailed information on this topic, we examined the effects of genistein by using an in vitro model of both, normal and "psoriasis-like" keratinocytes at this stage of our work exhaustively testing the selected flavonoid in a mono-treated experimental design. Gene expression studies revealed transcriptional changes that confirms known disease-associated pathways and highlights many psoriasis-related genes. Our results suggested that aberrant expression of genes contributing to the progress of psoriasis could be improved by the action of genistein. Genistein prevented "cytokine mix" as well as TNF-α-induced NF-κB nuclear translocation, with no effect on the PI3K signaling cascade, indicating the luck of turning this pathway into NF-κB activation. It could have attenuated TNF-α and LPS-induced inflammatory responses by suppressing ROS activation. Regardless of the type of keratinocyte stimulation used, reduction of cytokine IL-8, IL-20 and CCL2 production (both at RNA and protein level) following genistein treatment was visible. Because investigations of other groups supported our commentary on potential administration of genistein as a potential weapon in the armamentarium against psoriasis, it is believed that this paper should serve to encourage researchers to conduct further studies on this subject.
Audience	Academic
Author	Moskot, Marta Smolińska, Elwira Szczerkowska-Dobosz, Aneta Węgrzyn, Grzegorz Purzycka-Bohdan, Dorota Gabig-Cimińska, Magdalena Banecki, Bogdan Jakóbkiewicz-Banecka, Joanna
AuthorAffiliation	University of Catanzaro, ITALY 4 Department of Molecular Biology, University of Gdańsk, Gdańsk, Poland 2 Department of Physiology, Medical University of Gdańsk, Gdańsk, Poland 6 Department of Dermatology, Venereology and Allergology, Medical University of Gdańsk, Gdańsk, Poland 3 Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Laboratory of Molecular Biology, Gdańsk, Poland 5 Department of Molecular and Cellular Biology, Intercollegiate Faculty of Biotechnology UG-MUG, Gdańsk, Poland 1 Department of Medical Biology and Genetics, University of Gdańsk, Gdańsk, Poland
AuthorAffiliation_xml	– name: 3 Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Laboratory of Molecular Biology, Gdańsk, Poland – name: 6 Department of Dermatology, Venereology and Allergology, Medical University of Gdańsk, Gdańsk, Poland – name: University of Catanzaro, ITALY – name: 5 Department of Molecular and Cellular Biology, Intercollegiate Faculty of Biotechnology UG-MUG, Gdańsk, Poland – name: 1 Department of Medical Biology and Genetics, University of Gdańsk, Gdańsk, Poland – name: 2 Department of Physiology, Medical University of Gdańsk, Gdańsk, Poland – name: 4 Department of Molecular Biology, University of Gdańsk, Gdańsk, Poland
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BackLink	https://www.ncbi.nlm.nih.gov/pubmed/29444128$$D View this record in MEDLINE/PubMed
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Copyright	COPYRIGHT 2018 Public Library of Science 2018 Smolińska et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2018 Smolińska et al 2018 Smolińska et al
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Snippet	Due to its strong proliferation-reducing effects on keratinocytes, and also anti-inflammatory properties, the isoflavone genistein has already been proposed as...
SourceID	plos doaj pubmedcentral proquest gale pubmed crossref
SourceType	Open Website Open Access Repository Aggregation Database Index Database Enrichment Source
StartPage	e0192297
SubjectTerms	1-Phosphatidylinositol 3-kinase Activation Analysis Anti-inflammatory agents Biochemistry Biology and Life Sciences Biophysics Cytotoxicity Dermatology Epithelial cells Experimental design Fibroblasts Gene expression Genes Genetic aspects Genetics Genistein Inflammation Interleukin 20 Interleukin 8 Isoflavones Keratinocytes Kinases Laboratories Lipopolysaccharides Medicine and Health Sciences Metabolism Molecular biology Monocyte chemoattractant protein 1 NF-κB protein Nuclear transport Physiological aspects Psoriasis Research and Analysis Methods Ribonucleic acid RNA Signaling Skin Skin diseases Transcription Translocation Tumor necrosis factor-α
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Title	Molecular action of isoflavone genistein in the human epithelial cell line HaCaT
URI	https://www.ncbi.nlm.nih.gov/pubmed/29444128 https://www.proquest.com/docview/2021372926 https://www.proquest.com/docview/2002484034 https://pubmed.ncbi.nlm.nih.gov/PMC5812592 https://doaj.org/article/bfe7bd9d4c464cfd87a5b9a9c47fe888 http://dx.doi.org/10.1371/journal.pone.0192297
Volume	13
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