Psoriatic skin transcript phenotype: androgen/estrogen and cortisone/ cortisol imbalance with increasing DNA damage response

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dc.contributor.authorBaşar Kılıç, Şeyma
dc.contributor.authorTaheri, Serpil
dc.contributor.authorMehmetbeyoğlu Duman, Ecmel
dc.contributor.authorÖksüm Solak, Eda
dc.contributor.authorYılmaz Şükranlı, Zeynep
dc.contributor.authorRassoulzadegan, Minoo
dc.contributor.authorBorlu, Murat
dc.date.accessioned2024-09-03T05:27:41Z
dc.date.available2024-09-03T05:27:41Z
dc.date.issued2024
dc.departmentTıp Fakültesi
dc.description.abstractPatients prone to psoriasis suffer after a breakdown of the epidermal barrier and developpoorly healing lesions with abnormal proliferation of keratinocytes. Strong inflammatory reactions withgenotoxicity (short telomeres) suggest impaired immune defenses with DNA damage repair response(DDR) in patients with psoriasis. Recent evidence indicates the existence of crosstalk mechanismslinking the DDR machinery and hormonal signaling pathways that cooperate to influence bothprogressions of many diseases and responses to treatment. The aim of this study was to clarify whethersteroid biosynthesis and genomic stability markers are altered in parallel during the formation ofpsoriatic skin. Understanding the interaction of the steroid pathway and DNA damage response iscrucial to addressing underlying fundamental issues and managing resulting epidermal barrierdisruption in psoriasis. Methods: Skin (Lesional, non-lesional) and blood samples from twenty psoriasis patients and fifteen healthy volunteers were collected. Real-Time-PCR study was performed to assess levels of known transcripts such as: estrogen (ESR1, ESR2), androgen (AR), glucocorticoid/mineralocorticoid receptors (NR3C1, NR3C2), HSD11B1/HSD11B2, and DNA damage sensors (SMC1A, TREX1, TREX2, SSBP3, RAD1, RAD18, EXO1, POLH, HUS1). Results: We found that ESR1, ESR2, HSD11B1, NR3C1, NR3C2, POLH, and SMC1A transcripts were significantly decreased and AR, TREX1, RAD1, and SSBP3 transcripts were increased dramatically in the lesional skin compared to skin samples of controls. Conclusion: We found that the regulation of the steroidogenic pathway was disrupted in the lesional tissue of psoriasis patients and that a sufficient glucocorticoid and mineralocorticoid response did not form and the estrogen/androgen balance was altered in favour of androgens. We suggest that an increased androgen response in the presence of DDR increases the risk of developing psoriasis. Although this situation may be the cause or the consequence of a disruption of the epidermal barrier, our data suggest developing new therapeutic strategies.
dc.identifier.doi10.1007/s11033-024-09782-1
dc.identifier.issn0301-4851
dc.identifier.issue1en_US
dc.identifier.scopusqualityQ2
dc.identifier.urihttps:/dx.doi.org/10.1007/s11033-024-09782-1
dc.identifier.urihttps://hdl.handle.net/20.500.12451/12389
dc.identifier.volume51en_US
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer Science and Business Media B.V.
dc.relation.ispartofMolecular Biology Reports
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectGenome Integrity
dc.subjectPsoriasis
dc.subjectSteroidogenic Pathway
dc.subjectTranscript Profiles
dc.titlePsoriatic skin transcript phenotype: androgen/estrogen and cortisone/ cortisol imbalance with increasing DNA damage response
dc.typeArticle

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