Role of HMGB1 on the onset of preeclampsia

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dc.contributor.authorMehmet Yılmaz
dc.contributor.authorFikri Erdemci
dc.contributor.authorFırat Aşır
dc.contributor.authorFatih Taş
dc.contributor.authorTuğcan Korak
dc.contributor.authorAyşegül Aşır
dc.contributor.authorNizamettin Bozbay
dc.contributor.authorİbrahim Batmaz
dc.date.accessioned2025-06-03T06:58:43Z
dc.date.available2025-06-03T06:58:43Z
dc.date.issued2025-05-29
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü
dc.description.abstractBackground: The molecular mechanisms differentiating early-onset preeclampsia (EO-PE) from late-onset preeclampsia (LO-PE) remain unclear. High Mobility Group Box 1 (HMGB1), a pro-inflammatory cytokine involved in immune responses and oxidative stress, has emerged as a potential contributor to PE pathogenesis. Our aim was to investigate expression of HMGB1 in the placentas of EO- and LO-PE patients by immunohistochemical methods and in silico analysis. Methods: This experimental case-control study included 20 EO-PE, 20 LO-PE, and 20 normotensive control pregnant women. Placental samples underwent immunohistochemical staining to determine HMGB1 expression levels, which were analyzed semiquantitatively using ImageJ software. Bioinformatic analysis utilizing STRING and Cytoscape identified HMGB1-associated protein networks and pathways relevant to PE. Clinical and biochemical parameters were statistically analyzed. Results: HMGB1 expression was significantly elevated in placentas from EO-PE patients compared to both LO-PE and control groups (p < 0.05). Histopathological assessment indicated severe structural disruptions in EO-PE placentas, including increased fibrin deposition, vascular degeneration, and higher incidence of apoptotic cells. Bioinformatics revealed significant interactions of HMGB1 with cytokine signaling pathways (IL-4, IL-13, IL-10) and platelet-related pathways (platelet activation and aggregation). Clinically, EO-PE patients exhibited higher systemic inflammatory markers (CRP, WBC, NLR) and greater biochemical evidence of multi-organ dysfunction. Conclusions: This study identifies significantly increased HMGB1 placental expression predominantly in EO-PE, supporting its role in heightened inflammation and endothelial dysfunction characteristic of this subgroup, suggesting its potential as a biomarker and therapeutic target specifically for EO-PE.
dc.identifier.doi10.1186/s12884-025-07701-1
dc.identifier.issn1471-2393
dc.identifier.issue1
dc.identifier.pmid40442700
dc.identifier.urihttps://doi.org/10.1186/s12884-025-07701-1
dc.identifier.urihttps://hdl.handle.net/20.500.12604/8702
dc.identifier.volume25
dc.identifier.wosqualityQ1
dc.indekslendigikaynakPubMed
dc.institutionauthorTaş, Fatih
dc.language.isoen
dc.publisherSpringer Science and Business Media LLC
dc.relation.ispartofBMC Pregnancy and Childbirth
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectBioinformatics
dc.subjectHMGB1
dc.subjectHistopathology
dc.subjectInflammation
dc.subjectPlacenta.
dc.titleRole of HMGB1 on the onset of preeclampsia
dc.typejournal-article
oaire.citation.issue1
oaire.citation.volume25

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