Blood transcriptional signatures of gallstone pathogenesis in patients with cholelithiasis and choledocholithiasis

Basit Öğe Kaydı
dc.contributor.authorAlbayrak, Doğan
dc.contributor.authorDoğanlar, Oğuzhan
dc.contributor.authorKahya, Eyüp
dc.contributor.authorDoğan, Ayten
dc.contributor.authorDoğanlar, Zeynep Banu
dc.date.accessioned2024-06-12T10:05:38Z
dc.date.available2024-06-12T10:05:38Z
dc.date.issued2022
dc.departmentTrakya Üniversitesien_US
dc.description.abstractAim: Disease-specific molecular signalling in peripheral blood has the potential to inform on pathophysiological mechanisms of diseases. Here, we aimed to investigate the blood-based gene expression profiles that reflect disease-specific pathogenic mechanisms of gallstones, such as antioxidant defence, heat-shock responses, DNA damage and repair, ABC pump mechanisms, mucin signals, mitochondrial dysfunction and apoptosis in patients with Cholelithiasis (CHL) and Choledocholithiasis (CHDL). Materials and Methods: The relative fold-change in the mRNA expression levels of 73 genes were analysed using a gallstone-related qRT-PCR array in 10 control individuals, 24 CHL patients and 23 CHDL patients. Serum malondialdehyde levels was determined by thiobarbituric-acid reactive substance assays, and 8-hydroxy-2’-deoxyguanosine levels was determined by ELISA assays. Results: Our results showed that peripheral whole blood gene expression profile strongly reflects tissue specific molecular signalling in gallstone pathogenesis. The present findings of altered gene expressions including antioxidant defence (CuZn-SOD, CAT), heat shock protein (HSP70), DNA repair (MLH1 and RAD18), pro-apoptotic (P53, BAX, Cytc and Caspase 3), ABC transporter (ABCB1, ABCC2, and LRP1) and Mucin signals (MUCIN4, MUCIN5AC and MUCIN5B) point out to DNA damages via oxidative stress as well as deteriorating ABC types pump mechanisms and mucin signals in CHL and CHDL patients. Our findings may also suggest that activation of mitophagy activator, DRP1/hFIS1/PINK1 axis induced by oxidative stress and DNA damage may have a role in the pathogenesis of CHL and CHDL. Conclusion: Our results indicate that a blood-based gene expression signature has promising accuracy for monitorize pathogenesis of disease in CHL patients, CHDL patients and unaffected controls.en_US
dc.identifier.doi10.5455/annalsmedres.2022.01.043
dc.identifier.endpage939en_US
dc.identifier.issn2636-7688
dc.identifier.issue9en_US
dc.identifier.startpage930en_US
dc.identifier.trdizinid1130716en_US]
dc.identifier.urihttps://doi.org/10.5455/annalsmedres.2022.01.043
dc.identifier.urihttps://search.trdizin.gov.tr/yayin/detay/1130716
dc.identifier.urihttps://hdl.handle.net/20.500.14551/13548
dc.identifier.volume29en_US
dc.indekslendigikaynakTR-Dizinen_US
dc.language.isoenen_US
dc.relation.ispartofAnnals of Medical Researchen_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.titleBlood transcriptional signatures of gallstone pathogenesis in patients with cholelithiasis and choledocholithiasisen_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

TR-Dizin İndeksli Yayınlar Koleksiyonu