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Published ahead of print on February 14, 2003, doi:10.1165/rcmb.2002-0276OC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 2, August 2003, 172-179

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Submitted on November 27, 2002
Revised on February 11, 2003

Identification of Genes Promoting Angiogenesis in Mouse Lung by Transcriptional Profiling

Sorachai Srisuma1, Shyam S Biswal2, Wayne A Mitzner3, Sandra J Gallagher4, Kim H Mai2, and Elizabeth M Wagner5*

1 Physiology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand; Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA, 2 Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA, 3 Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA; Medicine, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA, 4 Medicine, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA, 5 Medicine, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA; Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA

* To whom correspondence should be addressed. E-mail: wagnerem{at}jhmi.edu.

A better understanding of the regulation of factors that promote angiogenesis may ultimately enable improved therapeutic control of this important process. In our previous studies, obstruction of the left pulmonary artery (LPA) in the mouse consistently induced the formation of a new vasculature, which developed from the visceral pleura and entered the upper left lung (ULL) directly within 5-6 days after ligation. No new vessels developed to the lower left lung (LLL), despite the initial ischemic stimulus being identical to that in the upper lung. Utilizing this unique model of angiogenesis, we have determined the temporal pattern of differential gene expression from two independent regions of the same lung - one where angiogenesis is induced and the other, where angiogenesis does not occur. By using microarray analysis and quantitative real time RT-PCR to compare signaling from these two lung regions in the first 3 days following ischemia, the findings reveal the important roles of ELR+ CXC chemokines as proangiogenic signals. Results also confirm that lung ischemia, rather than hypoxia is the essential trigger for angiogenesis. Genes involved in tissue remodeling, inflammation and injury were also upregulated in the proangiogenic upper lung. These altered profiles of expression in the early stage of lung ischemia show potential roles and interactions of the most important genes involved in promoting new blood vessel formation.




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