Pathology, research and practice · 2013
14-3-3 gene expression exerts isoform-dependent functions in sinonasal pathophysiology.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kataki Agapi, Alevizos Leonidas, Lazaris Andreas, Glustianou Georgia, Derventzi Anastasia, Giotakis Evagelos, Konstadoulakis Manousos, Yiotakis Ioannis
Аннотация
The expression profiles of 14-3-3β and θ isoforms, known to exert both oncogenic and antiapoptotic effects, were assessed in different entities of nasal pathophysiology. Flow cytometry and immunohistochemistry were used on paraffin-embedded sections of 51 inverted papillomas (IP), 26 nasal polyps (NP), 9 polyps with IP (NPIP) and 10 specimens of normal epithelium (NE). 14-3-3β expression was significantly upregulated in IP as compared with both NP (p=0.015) and NE (p=0.002). 14-3-3β was also increased in NPIP as compared with NE (p=0.008). 14-3-3β cytoplasmic staining was more pronounced in basal cells of the respiratory epithelium although serous glands and the vascular system were often positive as well. High 14-3-3β immunopositivity in IP patients concurred with increased proliferative activity shown by PCNA immunostaining (p=0.04). Expression of 14-3-3θ was also found increased in IP and NPIP patients, compared to NP (p=0.005, p=0.002 respectively) and NE (p=0.004 and p=0.001 respectively). 14-3-3θ cytoplasmic immunopositivity was detected in columnar epithelium, particularly in basal and subluminal cells, whereas no immunoreactivity was observed in NP and NE. Our results demonstrate differential expression of 14-3-3β and θ isoforms in sinonasal pathophysiology, supporting their implication, respectively, in the proliferative and inflammatory process engaged in the formation of IP.