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J Appl Physiol (October 6, 2005). doi:10.1152/japplphysiol.00029.2005
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Submitted on January 10, 2005
Accepted on October 1, 2005

Pulmonary ischemia induces lung remodeling and angiogenesis

Elizabeth M. Wagner1*, Irina Petrache1, Brian Schofield1, and Wayne Mitzner1

1 Department of Medicine and Environmental Health Sciences, Johns Hopkins University, Baltimore, MD, USA

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

Cellular remodeling during angiogenesis in the lung is poorly described. Furthermore, it is the systemic vasculature of and surrounding the lung that is proangiogenic when the pulmonary circulation becomes impaired. In a mouse model of chronic pulmonary thromboembolism, after left pulmonary artery ligation (LPAL), the intercostal vasculature in proximity to the ischemic lung proliferates and invades the lung (12). In the present study, we performed a detailed investigation of the kinetics of remodeling using histologic sections of the left lung of C57Bl/6J mice after LPAL (4 hrs - 20 days) or after sham surgery. New vessels were seen within the thickened visceral pleura 4 days after LPAL predominantly in the upper portion of the left lung. Connections between new vessels within the pleura and pulmonary capillaries were clearly discerned by 7 days after LPAL. The visceral pleura and the lung parenchyma showed intense tissue remodeling as evidenced by markedly elevated levels of both PCNA and TUNEL positive cells. Rapidly dividing cells were predominantly macrophages and type II pneumocytes. The increased apoptotic activity was further quantified by caspase-3 activity, which showed a 6-fold increase relative to naive lungs, by 24 hrs after LPAL. Since sham surgeries had little effect on measured parameters, we conclude that both thoracic wound healing and pulmonary ischemia are required for systemic neovascularization.




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