The role of p21 Waf1/Cip1 in large airway epithelium in smokers with and without COPD

作者: Giuseppina Chiappara , Mark Gjomarkaj , Alessia Virzì , Serafina Sciarrino , Maria Ferraro

DOI: 10.1016/J.BBADIS.2013.04.022

关键词: BiologySurvivinCancer researchCarboxyfluorescein succinimidyl esterEpitheliumCell growthRespiratory epitheliumCell cycleEpithelial MetaplasiaMetaplasia

摘要: Airway epithelium alterations, including squamous cell metaplasia, characterize smokers with and without chronic obstructive pulmonary disease (COPD). The p21 regulates apoptosis differentiation its role in COPD is largely unknown. Molecules regulating (cytoplasmic p21, caspase-3), cycle (nuclear p21), proliferation (Ki67/PCNA), metaplasia (survivin) central airways from (S), smokers-COPD (s-COPD) non-smokers (Controls) were studied. of cigarette smoke extracts (CSE) survivin, (caspase-3 annexin-V binding) was assessed a bronchial epithelial line (16HBE). Immunohistochemistry, image analysis surgical samples flow-cytometry carboxyfluorescein succinimidyl ester proliferative assay 16HBE with/without CSE applied. Cytoplasmic nuclear Ki67 expression significantly increased large airway S s-COPD comparison to Controls. Caspase-3 similar all the studied groups. correlated PCNA, expression. cytoplasmic survivin but not inhibited 16HBE. In COPD, inhibits apoptosis, promotes correlates thus representing potential pre-oncogenic hallmark.

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