The role of bronchial epithelial cell apoptosis in the pathogenesis of COPD

Basit Öğe Kaydı
dc.authoridBayraktar, Recep/0000-0002-8227-2055
dc.authoridBayram, Hasan/0000-0002-5236-766X
dc.authoridkahraman, demet/0000-0002-7038-3831
dc.contributor.authorGogebakan, B.
dc.contributor.authorBayraktar, R.
dc.contributor.authorUlasli, M.
dc.contributor.authorOztuzcu, S.
dc.contributor.authorTasdemir, D.
dc.contributor.authorBayram, H.
dc.date.accessioned2024-09-18T20:02:34Z
dc.date.available2024-09-18T20:02:34Z
dc.date.issued2014
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractThere is an increased airway inflammation in the pathogenesis of chronic obstructive pulmonary disease (COPD), and it has been suggested that there may also be problem in the apoptosis and renewal of cells. However, there are limited human airway cell studies, in particular those from larger airways such as bronchi. We cultured primary human bronchial epithelial cells (HBECs) from bronchial explants of smokers (n = 6) without COPD and smokers with COPD (n = 8). Apoptosis was studied by fluorescence activated cell sorting. qRT-PCR was used to assess mRNA expression for proteins involving apoptosis including p21(CIP1/WAF1), p53, caspase-8 and caspase-9. Although there was no difference in the rate of viable cells between cells from smokers and COPDs, the level of early apoptotic cells was significantly increased in COPD cells [mean +/- A standard error of mean (SEM) = 4.86 +/- A 3.2 %, p = 0.015] as compared to smokers (mean +/- A SEM = 2.71 +/- A 1.62 %). In contrast, the rate of late apoptotic cells was significantly decreased in COPD cells (mean +/- A SEM = 9.82 +/- A 5.71 %) comparing to smokers (mean +/- A SEM = 15.21 +/- A 5.08 %, p = 0.003). Although expression of mRNA for p21(CIP1/WAF1) and caspase-9 was similar in both groups, p53 and caspase-8 mRNA expression was significantly greater in COPD cells. These findings suggest that HBEC apoptosis is increased in COPD, and that this involves p53 and caspase-8 pathways.en_US
dc.description.sponsorshipResearch Fund of Gaziantep University [TF.11.32]en_US
dc.description.sponsorshipThis study is funded by The Research Fund of Gaziantep University with the Grant No.: TF.11.32.en_US
dc.identifier.doi10.1007/s11033-014-3403-3
dc.identifier.endpage5327en_US
dc.identifier.issn0301-4851
dc.identifier.issn1573-4978
dc.identifier.issue8en_US
dc.identifier.pmid24871992en_US
dc.identifier.scopus2-s2.0-84905097328en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage5321en_US
dc.identifier.urihttps://doi.org/10.1007/s11033-014-3403-3
dc.identifier.urihttps://hdl.handle.net/20.500.12483/7869
dc.identifier.volume41en_US
dc.identifier.wosWOS:000339910900047en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofMolecular Biology Reportsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApoptosisen_US
dc.subjectCaspasesen_US
dc.subjectCOPDen_US
dc.subjectPrimary bronchial epithelial cellsen_US
dc.subjectp21en_US
dc.subjectp53en_US
dc.titleThe role of bronchial epithelial cell apoptosis in the pathogenesis of COPDen_US
dc.typeArticleen_US

Dosyalar

Orijinal paket
Listeleniyor 1 - 1 / 1
[ N/A ]
İsim:
7869.pdf
Boyut:
696.89 KB
Biçim:
Adobe Portable Document Format
Açıklama:
Tam Metin / Full Text
İndir

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayınlar Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu