Genistein stimulates the viability and prevents myofibroblastic transformation in human trabecular meshwork cells stimulated by TGF-β

cris.virtual.author-orcid0000-0002-7182-6905
cris.virtual.author-orcid0000-0002-9011-8592
cris.virtual.author-orcid0000-0002-0081-7585
cris.virtual.author-orcid0000-0003-0715-0223
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cris.virtualsource.author-orcid325904ea-6775-4d8a-b846-0104d9ec20ca
cris.virtualsource.author-orcid5a92c57a-50a8-4d53-a17d-17ad767a350e
cris.virtualsource.author-orcidfa9a05b6-07fa-47e8-ae3d-8929da6881f3
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cris.virtualsource.author-orcid0c22ceb5-e5c6-4f5d-a0fd-8ec91a16efa9
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dc.abstract.enways to prevent/treat this entity is one of the main challenges of today’s ophthalmology. One of such solution seems to be biologically active substances of natural origin, such as genistein (GEN), which can affect the function of isolated trabecular meshwork by the inhibition of protein tyrosine kinase. However, the role of GEN in viability as well as myofibroblastic transformation in human trabecular meshwork cells stimulated by TGF-β is unknown. Using human trabecular meshwork cells (HTMCs) we investigated the effect of genistein on cell viability and myofibroblastic transformation stimulated by TGF-β1 and TGF-β2. Using Real-Time PCR, western blot and immunofluorescence we determined the effect on the expression changes of αSMA, TIMP1, collagen 1 and 3 at mRNA and protein level. We found that genistein increases the viability of HTMCs (1, 2, 3 μg/ml; P <0.05 and 4, 5, 10, 15, 20 μg/ml; P < 0.01). Moreover, we found that addition of 10, 15 and 20 μg/ml is able to prevent myofibroblastic transformation of HTMCs by decreasing αSMA, TIMP1, collagen 1 and 3 mRNA and protein expression (P < 0.01). Based on the obtained results, we can conclude that genistein is a potential factor that can prevent the myofibroblastic transformation of HTMCs accompanying glaucoma. Describing GEN influence on myofibroblastic transformation processes in HTMC allows us to conclude that it can be considered a potential therapeutic agent or a substance supporting treatment in patients with glaucoma.
dc.affiliationWydział Medycyny Weterynaryjnej i Nauk o Zwierzętach
dc.affiliationWydział Leśny i Technologii Drewna
dc.affiliation.instituteKatedra Fizjologii, Biochemii i Biostruktury Zwierząt
dc.affiliation.instituteKatedra Chemii
dc.contributor.authorWasilewicz, Robert
dc.contributor.authorWasilewicz, Julia
dc.contributor.authorPruszyńska-Oszmałek, Ewa
dc.contributor.authorStuper-Szablewska, Kinga
dc.contributor.authorLeciejewska, Natalia
dc.contributor.authorKołodziejski, Paweł Antoni
dc.date.accessioned2024-11-28T08:32:47Z
dc.date.available2024-11-28T08:32:47Z
dc.date.issued2024
dc.description.bibliographyil., bibliogr.
dc.description.financepublication_nocost
dc.description.financecost0,00
dc.description.if3,0
dc.description.points100
dc.description.reviewreview
dc.description.volume240
dc.identifier.doi10.1016/j.exer.2024.109806
dc.identifier.issn0014-4835
dc.identifier.urihttps://sciencerep.up.poznan.pl/handle/item/2119
dc.languageen
dc.relation.ispartofExperimental Eye Research
dc.relation.pagesart. 109806
dc.rightsClosedAccess
dc.sciencecloudsend
dc.subject.englaucoma
dc.subject.engenistein
dc.subject.enHTMCs
dc.subject.enhuman trabecular meshwork cells
dc.subject.enTGFs
dc.titleGenistein stimulates the viability and prevents myofibroblastic transformation in human trabecular meshwork cells stimulated by TGF-β
dc.typeJournalArticle
dspace.entity.typePublication
oaire.citation.volume240