Intrinsic pro-angiogenic status of cystic fibrosis airway epithelial cells

被引:26
作者
Verhaeghe, Catherine
Tabruyn, Sebastien P.
Oury, Cecile
Bours, Vincent [1 ]
Griffioen, Arian W.
机构
[1] Univ Liege, Human Genet Unit, GIGA Res, B-4000 Liege, Belgium
[2] Univ Maastricht, Dept Pathol, Angiogenesis Lab, GROW, Maastricht, Netherlands
关键词
angiogenesis; cystic fibrosis; lung inflammation; VEGF; endothelial cells; epithelial cells;
D O I
10.1016/j.bbrc.2007.02.166
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
Cystic fibrosis is a common genetic disorder characterized by a severe lung inflammation and fibrosis leading to the patient's death. Enhanced angiogenesis in cystic fibrosis (CF) tissue has been suggested, probably caused by the process of inflammation, as similarly described in asthma and chronic bronchitis. The present study demonstrates an intrinsic pro-angiogenic status of cystic fibrosis airway epithelial cells. Microarray experiments showed that CF airway epithelial cells expressed several angiogenic factors such as VEGF-A, VEGF-C, bFGF, and PLGF at higher levels than control cells. These data were confirmed by real-time quantitative PCR and, at the protein level, by ELISA. Conditioned media of these cystic fibrosis cells were able to induce proliferation, migration and sprouting of cultured primary endothelial cells. This report describes for the first time that cystic fibrosis epithelial cells have an intrinsic angiogenic activity. Since excess of angiogenesis is correlated with more severe pulmonary disease, our results could lead to the development of new therapeutic applications. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:745 / 749
页数:5
相关论文
共 26 条
[1]   Angiopoietin-1 decreases plasma leakage by reducing number and size of endothelial gaps in venules [J].
Baffert, F ;
Le, T ;
Thurston, G ;
McDonald, DM .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2006, 290 (01) :H107-H118
[2]   THE RELATIONSHIP BETWEEN INFECTION AND INFLAMMATION IN THE EARLY STAGES OF LUNG-DISEASE FROM CYSTIC-FIBROSIS [J].
BALOUGH, K ;
MCCUBBIN, M ;
WEINBERGER, M ;
SMITS, W ;
AHRENS, R ;
FICK, R .
PEDIATRIC PULMONOLOGY, 1995, 20 (02) :63-70
[3]   Anti-angiogenesis and anti-tumor activity of recombinant anginex [J].
Brandwijk, Ricardo J. M. G. E. ;
Dings, Ruud P. M. ;
van der Linden, Edith ;
Mayo, Kevin H. ;
Thijssen, Victor L. J. L. ;
Griffioen, Arjan W. .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2006, 349 (03) :1073-1078
[4]   VEGF as a key mediator of angiogenesis in cancer [J].
Carmeliet, P .
ONCOLOGY, 2005, 69 :4-10
[5]   Angiogenesis in life, disease and medicine [J].
Carmeliet, P .
NATURE, 2005, 438 (7070) :932-936
[6]   Anti-inflammatory effects of azithromycin in cystic fibrosis airway epithelial cells [J].
Cigana, Cristina ;
Nicolis, Elena ;
Pasetto, Matteo ;
Assael, Baroukh Maurice ;
Melotti, Paola .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2006, 350 (04) :977-982
[7]   Inflammation, infection, and pulmonary function in infants and young children with cystic fibrosis [J].
Dakin, CJ ;
Numa, AH ;
Wang, H ;
Morton, JR ;
Vertzyas, CC ;
Henry, RL .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2002, 165 (07) :904-910
[8]   Activation of NF-κB by adherent Pseudomonas aeruginosa in normal and cystic fibrosis respiratory epithelial cells [J].
DiMango, E ;
Ratner, AJ ;
Bryan, R ;
Tabibi, S ;
Prince, A .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (11) :2598-2605
[9]   Anti-angiogenesis therapy can overcome endothelial cell anergy and promote leukocyte-endothelium interactions and infiltration in tumors [J].
Dirkx, Anita E. M. ;
Egbrink, Mirjam G. A. oude ;
Castermans, Karolien ;
van der Schaft, Daisy W. J. ;
Thijssen, Victor L. J. L. ;
Dings, Ruud P. M. ;
Kwee, Lucy ;
Mayo, Kevin H. ;
Wagstaff, John ;
Steege, Jessica C. A. Bouma-ter ;
Griffioen, Arjan W. .
FASEB JOURNAL, 2006, 20 (06) :621-630
[10]   Massive hemoptysis in cystic fibrosis [J].
Flume, PA ;
Yankaskas, JR ;
Ebeling, M ;
Hulsey, T ;
Clark, LL .
CHEST, 2005, 128 (02) :729-738