Expression/Activation of PAR-1 in Airway Epithelial Cells of COPD Patients: Ex Vivo/In Vitro Study

被引:1
|
作者
Montalbano, Angela Marina [1 ]
Chiappara, Giuseppina [1 ]
Albano, Giusy Daniela [1 ]
Ferraro, Maria [1 ]
Di Sano, Caterina [1 ]
Vitulo, Patrizio [2 ]
Pipitone, Loredana [2 ]
Ricciardolo, Fabio Luigi Massimo [3 ]
Anzalone, Giulia [1 ]
Profita, Mirella [1 ]
机构
[1] Natl Res Council Italy CNR, Inst Biomed Res & Innovat IRIB, I-90146 Palermo, Italy
[2] Ist Mediterraneo Trapianti & Terapie Alta Special, I-90127 Palermo, Italy
[3] Univ Turin, Dept Clin & Biol Sci, I-10124 Turin, Italy
关键词
protease-activated receptor-1; inflammation; epithelial cells; cigarette smoke; COPD; OBSTRUCTIVE PULMONARY-DISEASE; PROTEASE-ACTIVATED RECEPTORS; THROMBIN RECEPTOR; LUNG; SMOKE; EXPRESSION; CLONING; REPAIR; INTERNALIZATION; PERMEABILITY;
D O I
10.3390/ijms221910703
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The role of PAR-1 expression and activation was described in epithelial cells from the central and distal airways of COPD patients using an ex vivo/in vitro model. PAR-1 immunoreactivity was studied in epithelial cells from surgical specimens of the central and distal airways of COPD patients and healthy control (HC). Furthermore, PAR-1 expression and activation were measured in both the human bronchial epithelial cell line (16HBE) and normal human bronchial epithelial cells (NHBEs) exposed to cigarette smoke extract (CSE) (10%) or thrombin. Finally, cell proliferation, apoptosis, and IL-8 release were detected in stimulated NHBEs. We identified higher levels of PAR-1 expression/activation in epithelial cells from the central airways of COPD patients than in HC. Active PAR-1 increased in epithelial cells from central and distal airways of COPD, with higher levels in COPD smokers (correlated with pack-years) than in COPD ex-smokers. 16HBE and NHBEs exposed to CSE or thrombin showed increased levels of active PAR-1 (localized in the cytoplasm) than baseline conditions, while NHBEs treated with thrombin or CSE showed increased levels of IL-8 proteins, with an additional effect when used in combination. Smoking habits generate the upregulation of PAR-1 expression/activation in airway epithelial cells, and promoting IL-8 release might affect the recruitment of infiltrating cells in the airways of COPD patients.
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页数:18
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